Mobile website
Volume 26,Issue 12,2019 Table of Contents
2019, 26(12):1297-1304.
Abstract:
Tumor is a complex systemic disease, involving abnormalities at multiple levels, such as DNA, RNA, protein and metabolite.According to the central rule, the derived omics methods are genomics, transcriptomics, proteomics and metabonomics. In the past few decades, there have been remarkable achievements in the single omics study of tumor, but the exact mechanism of tumor development is still unclear. In order to reveal the process of tumorigenesis and development in a more systematic way, the research of multiomics came into being, which promoted the transformation of tumor research paradigm from single parameter model to multi parameter system model. The integration of multi-omics methods is expected to clarify the mechanism of tumor occurrence and development, find biomarkers with diagnostic, prognostic and predictive performance, explore new treatment targets, and finally achieve predictive, preventive,and personalized medicine (PPPM). This paper reviews the research methods and progress of different omics techniques in tumor research, especially emphasizes the importance and scientific value of the integration of multiple omics techniques in tumor research and clinical related results.
Tumor is a complex systemic disease, involving abnormalities at multiple levels, such as DNA, RNA, protein and metabolite.According to the central rule, the derived omics methods are genomics, transcriptomics, proteomics and metabonomics. In the past few decades, there have been remarkable achievements in the single omics study of tumor, but the exact mechanism of tumor development is still unclear. In order to reveal the process of tumorigenesis and development in a more systematic way, the research of multiomics came into being, which promoted the transformation of tumor research paradigm from single parameter model to multi parameter system model. The integration of multi-omics methods is expected to clarify the mechanism of tumor occurrence and development, find biomarkers with diagnostic, prognostic and predictive performance, explore new treatment targets, and finally achieve predictive, preventive,and personalized medicine (PPPM). This paper reviews the research methods and progress of different omics techniques in tumor research, especially emphasizes the importance and scientific value of the integration of multiple omics techniques in tumor research and clinical related results.
2019, 26(12):1305-1310.
Abstract:
Objective: To investigate the expressionof proline-rich protein 11 (PRR11) in esophageal carcinoma (EC) tissues and to study it’s effect on the proliferation and metastasis of human EC TE-2 cells in vitro. Methods: Eighty patients were pathologically diagnosed with EC the Department of Thoracic Surgery of the Second Affiliated Hospital of Zhengzhou University from October 2016 to October 2018, and their surgically resected cancer tissues and corresponding para-cancerous tissues were collected for this study. qPCR was used to detect the expression of PRR11 mRNA in tissues or cells. Log-rank Test was used to analyzethe relationship between the expression of PRR11 in EC tissues and general data, histological type, lymphatic metastasis, depth of invasion and TNM stageof the EC patients. Kaplan-Meierplot was used to analyze the association between PRR11 mRNA and patients’prognosis. TE-2 cells were transfected with lentivirus shRNA to construct cell line with PRR11 knockout and corresponding control cell lines, as shPRR11#1,shPRR11#2 and control group. qPCR and WB assays were used to verify the mRNA and protein expressions of PRR11 in cell lines respectively.MTT was used to examine the proliferation of transfected cells, and Transwell experiments were used to detect cell invasion and migration. Results: The expression of PRR11 mRNA in EC was higher than that in para-cancer tissues (P<0.05). There was sig‐nificant correlation between PRR11 over-expression and histological type, lymphatic metastasis, depth of invasion and TNM stage(all P <0.05), and high PRR11 expression was significantly related with the poor prognosis of EC patients (P<0.05). The mRNA and protein expressions of PRR11 in cells of shPRR11#1 and shPRR11#2 groups were significantly lower than those in control group (all P<0.05).MTT assay showed that the proliferation of cells in shPRR11#1 and shPRR11#2 groups was significantly lower than that in the control group (P<0.05 or P<0.01). The results of Transwell invasion and migration assays showed that the average number of cells with in each field of viewin shPRR11#1 and shPRR11#2 groups was significantly lower than that in the control group (P<0.01). Conclusion: PRR11 is over-expressed in EC tissues and PRR11 over-expression is closely related to the occurrence, progression and prognosis of esophageal cancer. In vitro experiments have also demonstrated that knockdown of PRR11 can inhibit the proliferation, invasion and migration of EC. PRR11 can be used as a potential molecule marker and drug targets for EC.
Objective: To investigate the expressionof proline-rich protein 11 (PRR11) in esophageal carcinoma (EC) tissues and to study it’s effect on the proliferation and metastasis of human EC TE-2 cells in vitro. Methods: Eighty patients were pathologically diagnosed with EC the Department of Thoracic Surgery of the Second Affiliated Hospital of Zhengzhou University from October 2016 to October 2018, and their surgically resected cancer tissues and corresponding para-cancerous tissues were collected for this study. qPCR was used to detect the expression of PRR11 mRNA in tissues or cells. Log-rank Test was used to analyzethe relationship between the expression of PRR11 in EC tissues and general data, histological type, lymphatic metastasis, depth of invasion and TNM stageof the EC patients. Kaplan-Meierplot was used to analyze the association between PRR11 mRNA and patients’prognosis. TE-2 cells were transfected with lentivirus shRNA to construct cell line with PRR11 knockout and corresponding control cell lines, as shPRR11#1,shPRR11#2 and control group. qPCR and WB assays were used to verify the mRNA and protein expressions of PRR11 in cell lines respectively.MTT was used to examine the proliferation of transfected cells, and Transwell experiments were used to detect cell invasion and migration. Results: The expression of PRR11 mRNA in EC was higher than that in para-cancer tissues (P<0.05). There was sig‐nificant correlation between PRR11 over-expression and histological type, lymphatic metastasis, depth of invasion and TNM stage(all P <0.05), and high PRR11 expression was significantly related with the poor prognosis of EC patients (P<0.05). The mRNA and protein expressions of PRR11 in cells of shPRR11#1 and shPRR11#2 groups were significantly lower than those in control group (all P<0.05).MTT assay showed that the proliferation of cells in shPRR11#1 and shPRR11#2 groups was significantly lower than that in the control group (P<0.05 or P<0.01). The results of Transwell invasion and migration assays showed that the average number of cells with in each field of viewin shPRR11#1 and shPRR11#2 groups was significantly lower than that in the control group (P<0.01). Conclusion: PRR11 is over-expressed in EC tissues and PRR11 over-expression is closely related to the occurrence, progression and prognosis of esophageal cancer. In vitro experiments have also demonstrated that knockdown of PRR11 can inhibit the proliferation, invasion and migration of EC. PRR11 can be used as a potential molecule marker and drug targets for EC.
2019, 26(12):1311-1317.
Abstract:
Objective: To investigate the effect of down-regulation of miR-221 on cell proliferation and apoptosis of chronic myeloid leukemia (CML) K562 cells and its related regulatory mechanism. Methods: K562 cells were divided into control group, miRNA negative control (miR-NC) group, miR-221 inhibitor group, miR-221 inhibitor+ negative control siRNA (NC siRNA) group and miR-221 inhibitor+ SOCS3 siRNA group. The cells in the control group received no additional treatment. Cells in miR-NC group and miR-221 inhibitor group were transfected with miR-NC and miR-221 inhibitor, respectively. Cells in miR-221 inhibitor+NC siRNA group and miR-221 inhibitor+SOCS3 siRNA group were transfected with NC siRNA and SOCS3 siRNA, respectively, on the basis of successful transfection with miR-221 inhibitor. The transfection efficiency of miR-221 inhibitor was identified by qPCR. Cell viability in each group was measured by CCK-8 assay. Apoptosis in each group was detected by Annexin V-FITC/PI staining using a flow cytometry.The protein expressions of SOCS3, p-JAK1, p-JAK2, p-STAT3 and survivin in each group were detected by WB. Results: Compared with the control group, miR-221 expression was significantly down-regulated in miR-221 inhibitor group (P<0.01), cell viability was significantly reduced at 48 and 72 h after transfection (P<0.05 or P<0.01), the number of apoptotic cells was significantly increased (P<0.01), the expression of SOCS3 was significantly increased (P<0.01) and the expression levels of p-JAK1, p-JAK2, p-STAT3 and survivin were significantly reduced (all P<0.01). Compared with miR-221 inhibitor group, cell viability was significantly increased at 24,48 and 72 h after transfection (P<0.05 or P<0.01), the number of apoptotic cells was significantly decreased (P<0.01) and the expression levels of p-JAK1, p-JAK2, p-STAT3 and survivin were significantly increased in miR-221 inhibitor+SOCS3 siRNA group (all P<0.01). Conclusion: Down-regulation of miR-221 inhibits proliferation and promotes apoptosis of K562 cells, the mechanism of which may be related with up-regulating SOCS3 expression to suppress JAK-STAT3 signaling pathway.
Objective: To investigate the effect of down-regulation of miR-221 on cell proliferation and apoptosis of chronic myeloid leukemia (CML) K562 cells and its related regulatory mechanism. Methods: K562 cells were divided into control group, miRNA negative control (miR-NC) group, miR-221 inhibitor group, miR-221 inhibitor+ negative control siRNA (NC siRNA) group and miR-221 inhibitor+ SOCS3 siRNA group. The cells in the control group received no additional treatment. Cells in miR-NC group and miR-221 inhibitor group were transfected with miR-NC and miR-221 inhibitor, respectively. Cells in miR-221 inhibitor+NC siRNA group and miR-221 inhibitor+SOCS3 siRNA group were transfected with NC siRNA and SOCS3 siRNA, respectively, on the basis of successful transfection with miR-221 inhibitor. The transfection efficiency of miR-221 inhibitor was identified by qPCR. Cell viability in each group was measured by CCK-8 assay. Apoptosis in each group was detected by Annexin V-FITC/PI staining using a flow cytometry.The protein expressions of SOCS3, p-JAK1, p-JAK2, p-STAT3 and survivin in each group were detected by WB. Results: Compared with the control group, miR-221 expression was significantly down-regulated in miR-221 inhibitor group (P<0.01), cell viability was significantly reduced at 48 and 72 h after transfection (P<0.05 or P<0.01), the number of apoptotic cells was significantly increased (P<0.01), the expression of SOCS3 was significantly increased (P<0.01) and the expression levels of p-JAK1, p-JAK2, p-STAT3 and survivin were significantly reduced (all P<0.01). Compared with miR-221 inhibitor group, cell viability was significantly increased at 24,48 and 72 h after transfection (P<0.05 or P<0.01), the number of apoptotic cells was significantly decreased (P<0.01) and the expression levels of p-JAK1, p-JAK2, p-STAT3 and survivin were significantly increased in miR-221 inhibitor+SOCS3 siRNA group (all P<0.01). Conclusion: Down-regulation of miR-221 inhibits proliferation and promotes apoptosis of K562 cells, the mechanism of which may be related with up-regulating SOCS3 expression to suppress JAK-STAT3 signaling pathway.
2019, 26(12):1318-1323.
Abstract:
Objective: To investigate the therapeutic effect of dendritic cell-induced killer cells (DC-CIK) combined with 5-fluorouracil (5-FU) and loaded with CD133 + HT-29 cell lysate or RNA on mice bearing colon cancer HT-29 cell transplanted tumor, and to explore the underlying mechanism. Methods: Colon cancer xenograft model was established in BALB /c nude mice by using human colon cancer HT-29 cells at logarithmic growth phase; Antigen-free DC-CIK, 5-FU+DC-CIK, R+DC-CIK (loaded with total RNA of CD133 + cells), L+DC-CIK (loaded with CD133 + cell lysate), 5-FU and normal saline were respectively injected into transplanted mice,and the treatment efficacies on the growth of transplanted tumor in each group after three treatment cycles were observed, and the tumor growth curve was drawn. The nude mice were sacrificed by cervical dislocation and the tumor volume and body weight were measured.qPCR was used to detect the expression of AKT mRNA in transplanted tumor tissue, and WB was used to detect the expression of phosphorylated AKT protein. Results: After treatment, the body mass of nude mice in R+DC-CIK group, L+DC-CIK group and 5-FU+DC-CIK group increased steadily, while the body mass of nude mice in DC-CIK group and 5-FU group decreased gradually; the tumor growth speed of nude mice in R+DC-CIK group, 5-FU+DC-CIK group and L+DC-CIK group was significantly slower than that of the control group (P<0.05). Compared with 5-FU and DC-CIK alone, the combined treatment with loaded lysate/RNA had more sig‐nificant effect on mRNA and protein expressions of AKT(P<0.05). Conclusion: The effect of DC-CIKwith different loading or its combination with 5-FU is better than that of chemotherapy alone. One of the mechanisms is related to the down-regulation of AKT level.
Objective: To investigate the therapeutic effect of dendritic cell-induced killer cells (DC-CIK) combined with 5-fluorouracil (5-FU) and loaded with CD133 + HT-29 cell lysate or RNA on mice bearing colon cancer HT-29 cell transplanted tumor, and to explore the underlying mechanism. Methods: Colon cancer xenograft model was established in BALB /c nude mice by using human colon cancer HT-29 cells at logarithmic growth phase; Antigen-free DC-CIK, 5-FU+DC-CIK, R+DC-CIK (loaded with total RNA of CD133 + cells), L+DC-CIK (loaded with CD133 + cell lysate), 5-FU and normal saline were respectively injected into transplanted mice,and the treatment efficacies on the growth of transplanted tumor in each group after three treatment cycles were observed, and the tumor growth curve was drawn. The nude mice were sacrificed by cervical dislocation and the tumor volume and body weight were measured.qPCR was used to detect the expression of AKT mRNA in transplanted tumor tissue, and WB was used to detect the expression of phosphorylated AKT protein. Results: After treatment, the body mass of nude mice in R+DC-CIK group, L+DC-CIK group and 5-FU+DC-CIK group increased steadily, while the body mass of nude mice in DC-CIK group and 5-FU group decreased gradually; the tumor growth speed of nude mice in R+DC-CIK group, 5-FU+DC-CIK group and L+DC-CIK group was significantly slower than that of the control group (P<0.05). Compared with 5-FU and DC-CIK alone, the combined treatment with loaded lysate/RNA had more sig‐nificant effect on mRNA and protein expressions of AKT(P<0.05). Conclusion: The effect of DC-CIKwith different loading or its combination with 5-FU is better than that of chemotherapy alone. One of the mechanisms is related to the down-regulation of AKT level.
LUO Mei
,
ZHOU Jianjiang
,
WANG Qinrong
,
YANG Liping
,
CHEN Xueshu
,
LONG Niya
,
XIE Yuan
,
ZHAO Yan
2019, 26(12):1324-1330.
Abstract:
Objective：To study the effect of silencing DKK1 (Dickkopf1) gene on the proliferation, cell cycle and apoptosis of gastric cancer AGS cells and the action mechanism. Methods：The DKK1-shRNA vector was constructed and transfected into AGS cells. The stably transfected cell lines were screened. The total protein and RNA of the transfected cells were extracted and the mRNA and protein expressions of DKK1 were detected by qPCR and WB, respectively. The experiment was divided into blank control group (Control),negative control group (shNC) and DKK1 silence group (DKK1-shRNA). CCK8 assay was used to detect the proliferation of AGS cells of each group cultured for 0, 24, 48, 72, 96, 120 and 144 h, and flow cytometry was used to analyze the cell cycle and apoptosis in each group. The relationship between DKK1 and clinicopathological features of gastric cancer was analyzed after searching HPA database.Results：The gastric cancer AGS cells with stable DKK1 gene knockdown was successfully established, and it was confirmed that the mRNA and proteinexpressions of DKK1 in DKK1-shRNA group decreased by 72% and 47%, respectively, compared to shNC group (all P<0.05). The cell proliferation curve showed that, the cell proliferation in DKKl-shRNA group significantly decreased after 72 hour of culture compared with that in control and shNC groups (P<0.05). The cell number of S phase decreased from 32.06% to 25.87%,while the number of G2/M phase increased from 8.49% to 21.26% compared with shNC group (all P<0.05). The number of apoptotic cells also statistically increased from 10.34% to 20.65% (all P<0.05). The data of HPA database showed that DKK1 mRNA level in gastric cancer tissues was significantly higher than that in normal tissues, and the high expression of DKK1 mRNA was negatively correlat‐ed with the survival rate of gastric cancer patients. Conclusion: Silencing DKK1 gene can inhibit the proliferation of gastric cancer cells, arrest cells in G2/M phase and promote cell apoptosis. DKK1 plays a pro-carcinogenic effect in gastric cancer.
Objective：To study the effect of silencing DKK1 (Dickkopf1) gene on the proliferation, cell cycle and apoptosis of gastric cancer AGS cells and the action mechanism. Methods：The DKK1-shRNA vector was constructed and transfected into AGS cells. The stably transfected cell lines were screened. The total protein and RNA of the transfected cells were extracted and the mRNA and protein expressions of DKK1 were detected by qPCR and WB, respectively. The experiment was divided into blank control group (Control),negative control group (shNC) and DKK1 silence group (DKK1-shRNA). CCK8 assay was used to detect the proliferation of AGS cells of each group cultured for 0, 24, 48, 72, 96, 120 and 144 h, and flow cytometry was used to analyze the cell cycle and apoptosis in each group. The relationship between DKK1 and clinicopathological features of gastric cancer was analyzed after searching HPA database.Results：The gastric cancer AGS cells with stable DKK1 gene knockdown was successfully established, and it was confirmed that the mRNA and proteinexpressions of DKK1 in DKK1-shRNA group decreased by 72% and 47%, respectively, compared to shNC group (all P<0.05). The cell proliferation curve showed that, the cell proliferation in DKKl-shRNA group significantly decreased after 72 hour of culture compared with that in control and shNC groups (P<0.05). The cell number of S phase decreased from 32.06% to 25.87%,while the number of G2/M phase increased from 8.49% to 21.26% compared with shNC group (all P<0.05). The number of apoptotic cells also statistically increased from 10.34% to 20.65% (all P<0.05). The data of HPA database showed that DKK1 mRNA level in gastric cancer tissues was significantly higher than that in normal tissues, and the high expression of DKK1 mRNA was negatively correlat‐ed with the survival rate of gastric cancer patients. Conclusion: Silencing DKK1 gene can inhibit the proliferation of gastric cancer cells, arrest cells in G2/M phase and promote cell apoptosis. DKK1 plays a pro-carcinogenic effect in gastric cancer.
2019, 26(12):1331-1336.
Abstract:
Objective: To investigate the effect of lncRNA SBF2-AS1 on epithelial-mesenchymal transition (EMT) of cervical cancer HeLa cell via regulating miR-140-5p/VEGFA (vascular endothelial growth factor A) axis. Methods: After cell culture and transfection,the cells were divided into 5 groups: NC group, miR-140-5p mimic group, miR-140-5p mimic+pcDNA-VEGFA group, si-lncRNA SBF2-AS1+pcDNA-VEGFA group and si-lncRNA SBF2-AS1+miR-140-5p mimic group. The expression level of lncRNA SBF2-AS1 in cervical cancer tissues and cell lines was detected by qPCR. The targeted relationship between lncRNA SBF2-AS1, miR-140-5p and VEGFA was confirmed by Dual luciferase reporter gene assay. The expression levels of VEGFA and EMT-related proteins N-cadherin,Vimentin and E-cadherin in HeLa cells were detected by WB. The invasion and migration of HeLa cells were detected by Transwell.Results: lncRNA SBF2-AS1 was highly expressed in cervical cancer tissues and cell lines (P<0.05 or P<0.01). Dual luciferase reporter gene assay confirmed that lncRNA SBF2-AS1 targetedly combined with miR-140-5p and VEGFA was a target gene of miR-140-5p (P<0.05). Knockdown of lncRNA SBF2-AS1 inhibited invasion and migration as well as EMT of HeLa cells. Further experiment confirmed that lncRNA SBF2-AS1 up-regulated the expression level of VEGFA via miR-140-5p, thereby promoting invasion, migration and EMT of HeLa cells. Conclusion: lncRNA SBF2-AS1 promotes EMT of HeLa cells via miR-140-5p/VEGFA axis.
Objective: To investigate the effect of lncRNA SBF2-AS1 on epithelial-mesenchymal transition (EMT) of cervical cancer HeLa cell via regulating miR-140-5p/VEGFA (vascular endothelial growth factor A) axis. Methods: After cell culture and transfection,the cells were divided into 5 groups: NC group, miR-140-5p mimic group, miR-140-5p mimic+pcDNA-VEGFA group, si-lncRNA SBF2-AS1+pcDNA-VEGFA group and si-lncRNA SBF2-AS1+miR-140-5p mimic group. The expression level of lncRNA SBF2-AS1 in cervical cancer tissues and cell lines was detected by qPCR. The targeted relationship between lncRNA SBF2-AS1, miR-140-5p and VEGFA was confirmed by Dual luciferase reporter gene assay. The expression levels of VEGFA and EMT-related proteins N-cadherin,Vimentin and E-cadherin in HeLa cells were detected by WB. The invasion and migration of HeLa cells were detected by Transwell.Results: lncRNA SBF2-AS1 was highly expressed in cervical cancer tissues and cell lines (P<0.05 or P<0.01). Dual luciferase reporter gene assay confirmed that lncRNA SBF2-AS1 targetedly combined with miR-140-5p and VEGFA was a target gene of miR-140-5p (P<0.05). Knockdown of lncRNA SBF2-AS1 inhibited invasion and migration as well as EMT of HeLa cells. Further experiment confirmed that lncRNA SBF2-AS1 up-regulated the expression level of VEGFA via miR-140-5p, thereby promoting invasion, migration and EMT of HeLa cells. Conclusion: lncRNA SBF2-AS1 promotes EMT of HeLa cells via miR-140-5p/VEGFA axis.
2019, 26(12):1337-1344.
Abstract:
Objective: To explore the effect of glycyrrhizin (GA) on the proliferation, invasion and migration of non-small cell lung cancer HCC827 and A549 cells via regulating miR-142/ZEB1 (Zinc finger E-box-binding homeobox 1) axis. Methods: After being cultured and transfected, HCC827 and A549 cells were divided into 4 groups: NC group (untransfected+3 mmol/L GA), miR-142 inhibitor group (miR-142 knockdown+3 mmol/L GA), pcDNA3.1-ZEB1 group (ZEB1 over-expression+3 mmol/L GA) and pcDNA3.1-ZEB1+miR-142 mimic group (ZEB1 over-expression+miR-142+3 mmol/L GA). qPCR was used to detect the expression level of miR-142 in HCC827 and A549 cells treated with different concentrations of GA. MTT and Transwell assays were used to examine the proliferation,invasion and migration of HCC827 and A549 cells. WB was used to detect the expression level of ZEB1 protein in HCC827 and A549 cells. Dual-luciferase reporter gene assay was used to explore the relationship between miR-142 and ZEB1. Results: GA significantly inhibited the proliferation, invasion and migration of HCC827 and A549 cells, and up-regulated the expression level of miR-142 (P<0.05 or P<0.01). Dual-luciferase reporter gene assay showed that miR-142 could targetedly combine with 3'-UTR of ZEB1 and downregulate the expression of ZEB1 (P<0.05 or P<0.01). Further experiment validated that GA inhibited ZEB1 expression via up-regulating miR-142, thus suppressed proliferation, invasion and migration of HCC827 and A549 cells (P<0.05 or P<0.01). Conclusion: GA inhibits the proliferation, invasion and migration of NSCLC HCC827 and A549 cells, the mechanism of which is that GA inhibits the malignant biological behavior of NSCLC HCC827 and A549 cells via up-regulating the inhibition effect of miR-142 on ZEB1.
Objective: To explore the effect of glycyrrhizin (GA) on the proliferation, invasion and migration of non-small cell lung cancer HCC827 and A549 cells via regulating miR-142/ZEB1 (Zinc finger E-box-binding homeobox 1) axis. Methods: After being cultured and transfected, HCC827 and A549 cells were divided into 4 groups: NC group (untransfected+3 mmol/L GA), miR-142 inhibitor group (miR-142 knockdown+3 mmol/L GA), pcDNA3.1-ZEB1 group (ZEB1 over-expression+3 mmol/L GA) and pcDNA3.1-ZEB1+miR-142 mimic group (ZEB1 over-expression+miR-142+3 mmol/L GA). qPCR was used to detect the expression level of miR-142 in HCC827 and A549 cells treated with different concentrations of GA. MTT and Transwell assays were used to examine the proliferation,invasion and migration of HCC827 and A549 cells. WB was used to detect the expression level of ZEB1 protein in HCC827 and A549 cells. Dual-luciferase reporter gene assay was used to explore the relationship between miR-142 and ZEB1. Results: GA significantly inhibited the proliferation, invasion and migration of HCC827 and A549 cells, and up-regulated the expression level of miR-142 (P<0.05 or P<0.01). Dual-luciferase reporter gene assay showed that miR-142 could targetedly combine with 3'-UTR of ZEB1 and downregulate the expression of ZEB1 (P<0.05 or P<0.01). Further experiment validated that GA inhibited ZEB1 expression via up-regulating miR-142, thus suppressed proliferation, invasion and migration of HCC827 and A549 cells (P<0.05 or P<0.01). Conclusion: GA inhibits the proliferation, invasion and migration of NSCLC HCC827 and A549 cells, the mechanism of which is that GA inhibits the malignant biological behavior of NSCLC HCC827 and A549 cells via up-regulating the inhibition effect of miR-142 on ZEB1.
2019, 26(12):1345-1349.
Abstract:
Objective:To explore the mechanism by which SRY-related high mobility group-box 9 (SOX9) promotes the epithelial mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC) A549 cells via the Wnt/β-catenin pathway. Methods: The human NSCLC A549 cell line was divided into three groups: OE-NC group, OE-SOX9 group and OE-SOX9+XAV-939 group. The cells in OESOX9 group were transfected with SOX9 pcDNA plasmid to up-regulate the expression level of SOX9; The cells in OE-SOX9+XAV-939 group were transfected with SOX9 pcDNA plasmid while the β-catenin inhibitor XAV-939 (1.0 μmol/L) was added to the medium.qPCR was used to detect SOX9 mRNA levels; CCK-8 was used to examine the proliferation of A549 cells; Wound-healing assay and Transwell chamber assay were used to detect the migration and invasion of A549 cells, respectively; and WB was used to detect protein expressions of SOX9, β-catenin, E-cadherin, γ-catenin, N-cadherin and vimentin. Results: The mRNA and protein levels of SOX9 in OE-SOX9 group and OE-SOX9+XAV-939 group were significantly higher than those in the OE-NC group after transfection (all P<0.05), while there was no significant difference between the OE-SOX9 group and the OE-SOX9+XAV-939 group (P>0.05). The proliferation,migration and invasion of cells in OE-SOX9 group were significantly higher than those in OE-NC group; however, those abilities in OE-SOX9+XAV-939 group were significantly lower than those in OE-SOX9 group (all P<0.05). The level of β-catenin protein in OE-SOX9 group was significantly higher than that in the OE-NC group, while the level of β-catenin protein in OE-SOX9+XAV-939 group was lower than that in OE-SOX9 group (all P<0.05). Compared with the OE-NC group, the levels of phenotypic markers of epithelial cells, E-cadherin and γ-catenin, were down-regulated, and the phenotypic markers of mesenchymal cells, N-cadherin and vimen‐tin, were up-regulated in cells of OE-SOX9 group; however, E-cadherin and γ-catenin were higher, and N-cadherin and vimentin were lower in OE-SOX9+XAV-939 group than those in OE-SOX9 group (all P<0.05). Conclusion: SOX9 could promote proliferation, migration and EMT of NSCLC A549 cells by activating the Wnt/β-catenin pathway.
Objective:To explore the mechanism by which SRY-related high mobility group-box 9 (SOX9) promotes the epithelial mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC) A549 cells via the Wnt/β-catenin pathway. Methods: The human NSCLC A549 cell line was divided into three groups: OE-NC group, OE-SOX9 group and OE-SOX9+XAV-939 group. The cells in OESOX9 group were transfected with SOX9 pcDNA plasmid to up-regulate the expression level of SOX9; The cells in OE-SOX9+XAV-939 group were transfected with SOX9 pcDNA plasmid while the β-catenin inhibitor XAV-939 (1.0 μmol/L) was added to the medium.qPCR was used to detect SOX9 mRNA levels; CCK-8 was used to examine the proliferation of A549 cells; Wound-healing assay and Transwell chamber assay were used to detect the migration and invasion of A549 cells, respectively; and WB was used to detect protein expressions of SOX9, β-catenin, E-cadherin, γ-catenin, N-cadherin and vimentin. Results: The mRNA and protein levels of SOX9 in OE-SOX9 group and OE-SOX9+XAV-939 group were significantly higher than those in the OE-NC group after transfection (all P<0.05), while there was no significant difference between the OE-SOX9 group and the OE-SOX9+XAV-939 group (P>0.05). The proliferation,migration and invasion of cells in OE-SOX9 group were significantly higher than those in OE-NC group; however, those abilities in OE-SOX9+XAV-939 group were significantly lower than those in OE-SOX9 group (all P<0.05). The level of β-catenin protein in OE-SOX9 group was significantly higher than that in the OE-NC group, while the level of β-catenin protein in OE-SOX9+XAV-939 group was lower than that in OE-SOX9 group (all P<0.05). Compared with the OE-NC group, the levels of phenotypic markers of epithelial cells, E-cadherin and γ-catenin, were down-regulated, and the phenotypic markers of mesenchymal cells, N-cadherin and vimen‐tin, were up-regulated in cells of OE-SOX9 group; however, E-cadherin and γ-catenin were higher, and N-cadherin and vimentin were lower in OE-SOX9+XAV-939 group than those in OE-SOX9 group (all P<0.05). Conclusion: SOX9 could promote proliferation, migration and EMT of NSCLC A549 cells by activating the Wnt/β-catenin pathway.
CAI Jingjing
,
LI Hongsheng
,
SHEN Zhenghai
,
MA Luyao
,
LI Quan
,
DU Yaqian
,
LIU Junxi
,
WANG Xiaoxiong
,
GUO Yinjin
,
ZHOU Yongchun
2019, 26(12):1350-1355.
Abstract:
Objective: To detect the mutation of epidermal growth factor receptor (EGFR) gene in peripheral blood of non-small cell lung cancer (NSCLC) patients in Yunnan area with Super-ARMS, and to explore its correlation with clinicopathological characteristics.Methods: A total of 222 blood samples from patients with NSCLC were collected between January 2017 to December 2018 in the Molecular Diagnostic Center of Yunnan Cancer Hospital. The EGFR gene mutation in peripheral blood samples was detected by Super-ARMS, and the relationship between EGFR gene mutation and clinicopathological features was analyzed. Meanwhile, the independent risk factors influencing EFGR mutation were also analyzed. Results: In the peripheral blood of 222 NSCLC patients, there were 81 cases (36.5%) with EGFR gene mutation. Among them, exon 19 deletion and L858R gene point mutation were the most common (75.3%of total mutation); female patients had a higher mutation rate than male patients (45.9% vs 27.0%); patients <60 years old had a higher incidence of mutation than patients ≥60 years old (43.2% vs 28.8%) (P<0.05 or P<0.01); moreover, patients with no history of smoking,no history of radical surgery, adenocarcinoma, advanced stage and no history of chemotherapy had higher incidence of EGFR mutation (43.9% vs 21.6%, 39.2% vs 21.2%, 43.9% vs 4.8%, 39.7% vs 23.3% and 44.0% vs 23.5%) (P<0.05 or P<0.01). Multivariate logistic analysis showed that young, no smoking history, adenocarcinoma and no surgical history were independent risk factors for EGFR gene mutation (all P<0.01). Conclusion: In the peripheral blood of patients with NSCLC in Yunnan, the mutation rate of EGFR gene is higher in patients with age<60 years old, adenocarcinoma and non-smoking. Super-ARMS method is more sensitive in the detection of EGFR mutation in peripheral blood of lung cancer patients.
Objective: To detect the mutation of epidermal growth factor receptor (EGFR) gene in peripheral blood of non-small cell lung cancer (NSCLC) patients in Yunnan area with Super-ARMS, and to explore its correlation with clinicopathological characteristics.Methods: A total of 222 blood samples from patients with NSCLC were collected between January 2017 to December 2018 in the Molecular Diagnostic Center of Yunnan Cancer Hospital. The EGFR gene mutation in peripheral blood samples was detected by Super-ARMS, and the relationship between EGFR gene mutation and clinicopathological features was analyzed. Meanwhile, the independent risk factors influencing EFGR mutation were also analyzed. Results: In the peripheral blood of 222 NSCLC patients, there were 81 cases (36.5%) with EGFR gene mutation. Among them, exon 19 deletion and L858R gene point mutation were the most common (75.3%of total mutation); female patients had a higher mutation rate than male patients (45.9% vs 27.0%); patients <60 years old had a higher incidence of mutation than patients ≥60 years old (43.2% vs 28.8%) (P<0.05 or P<0.01); moreover, patients with no history of smoking,no history of radical surgery, adenocarcinoma, advanced stage and no history of chemotherapy had higher incidence of EGFR mutation (43.9% vs 21.6%, 39.2% vs 21.2%, 43.9% vs 4.8%, 39.7% vs 23.3% and 44.0% vs 23.5%) (P<0.05 or P<0.01). Multivariate logistic analysis showed that young, no smoking history, adenocarcinoma and no surgical history were independent risk factors for EGFR gene mutation (all P<0.01). Conclusion: In the peripheral blood of patients with NSCLC in Yunnan, the mutation rate of EGFR gene is higher in patients with age<60 years old, adenocarcinoma and non-smoking. Super-ARMS method is more sensitive in the detection of EGFR mutation in peripheral blood of lung cancer patients.
2019, 26(12):1356-1362.
Abstract:
Objective: To explore the expressions of melanoma antigen (MAGE) -A9, -A11 and Ki67 in laryngeal squamous cell carcinoma (LSCC) tissues, and to analyze their correlation with clinicopathological features and the prognosisof LSCC patients. Methods: A total of 73 pairs of LSCC tissuesand corresponding para-cancerous tissues resected from LSCC patients, who were treated at the Fourth Hospital of Hebei Medical University from 2012 to 2014,were collected for this study. At the same time, testicular tissues from 3 patients with prostate cancer after castration were selected as positive control. The protein expressions of MAGE-A9, MAGE-A11 and Ki67 in LSCC tissues and its para-cancerous tissues were detected by immunohistochemistry. Results: The expression rates of MAGEA9,MAGE-A11 protein and Ki67 in LSCC tissues were 47.94% (35/73), 49.32% (36/73) and 46.58% (34/73) respectively, which were significantly higher than those in para-cancerous tissues. The protein expressions of MAGE-A9 and MAGE-A11 were correlated with clinical stage and lymphatic metastasis of LSCC (P<0.05). The expression of Ki67LI was correlated with tumor size, clinical stage and lymphatic metastasis of LSCC (P<0.05). The correlation analysis showed that the expressions of MAGE-A9 and MAGE-A11 were positively correlated with Ki67 (r=0.258, P＝0.027; r=0.672, P=0.001). Kaplan-Meier survival curve analysis showed that the survival rates of patients with high expression of MAGE-A9 protein (P=0.009), MAGE-A11 protein (P=0.031) and Ki67LI (P=0.040) were signifi‐cantly lower than those with low expressions. And the survival time of patients with both high expressions of MAGE-A9 and Ki67LI (P=0.001) or both high expressions of MAGE-A11 and Ki67 (P=0.001) was significantly shorter than that of patients with low expression (both or single). Univariate and multivariate Cox regression analysis further indicated that MAGE-A9 protein (P=0.028) and MAGE-A11 protein (P=0.042) were independent prognostic factors for overall survival of LSCC patients. Conclusion: MAGE-A9,MAGE-A11 and Ki67 are tumor-associated antigens of LSCC, which can be used as prognostic indicators for LSCC.
Objective: To explore the expressions of melanoma antigen (MAGE) -A9, -A11 and Ki67 in laryngeal squamous cell carcinoma (LSCC) tissues, and to analyze their correlation with clinicopathological features and the prognosisof LSCC patients. Methods: A total of 73 pairs of LSCC tissuesand corresponding para-cancerous tissues resected from LSCC patients, who were treated at the Fourth Hospital of Hebei Medical University from 2012 to 2014,were collected for this study. At the same time, testicular tissues from 3 patients with prostate cancer after castration were selected as positive control. The protein expressions of MAGE-A9, MAGE-A11 and Ki67 in LSCC tissues and its para-cancerous tissues were detected by immunohistochemistry. Results: The expression rates of MAGEA9,MAGE-A11 protein and Ki67 in LSCC tissues were 47.94% (35/73), 49.32% (36/73) and 46.58% (34/73) respectively, which were significantly higher than those in para-cancerous tissues. The protein expressions of MAGE-A9 and MAGE-A11 were correlated with clinical stage and lymphatic metastasis of LSCC (P<0.05). The expression of Ki67LI was correlated with tumor size, clinical stage and lymphatic metastasis of LSCC (P<0.05). The correlation analysis showed that the expressions of MAGE-A9 and MAGE-A11 were positively correlated with Ki67 (r=0.258, P＝0.027; r=0.672, P=0.001). Kaplan-Meier survival curve analysis showed that the survival rates of patients with high expression of MAGE-A9 protein (P=0.009), MAGE-A11 protein (P=0.031) and Ki67LI (P=0.040) were signifi‐cantly lower than those with low expressions. And the survival time of patients with both high expressions of MAGE-A9 and Ki67LI (P=0.001) or both high expressions of MAGE-A11 and Ki67 (P=0.001) was significantly shorter than that of patients with low expression (both or single). Univariate and multivariate Cox regression analysis further indicated that MAGE-A9 protein (P=0.028) and MAGE-A11 protein (P=0.042) were independent prognostic factors for overall survival of LSCC patients. Conclusion: MAGE-A9,MAGE-A11 and Ki67 are tumor-associated antigens of LSCC, which can be used as prognostic indicators for LSCC.
2019, 26(12):1363-1370.
Abstract:
Objective: To explore the mechanism of lncRNA XIST (XIST) regulating the biological behaviors of colorectal cancer HCT-8 cells via miR-32-5p/EZH2 (enhancer of Zeste homolog 2) axis. Methods: A total of 28 pairs of cancer tissues and corresponding para-cancerous tissues form colorectal cancer patients with complete clinical data were collected from the Colorectal and Anal Surgery,Xiangya Hospital of Central South University during July 2014 and August 2018. The expression levels of lncRNA XIST and miR-32-5p in colorectal cancer tissues and cell lines were detected by qPCR. The targeted relationship between lncRNA XIST, miR-32-5p and EZH2 was verified by dual luciferase reporter gene, and the expression level of EZH2 was further detected by WB. The proliferation,migration and apoptosis of HCT-8 cells were detected by CCK-8, Transwell and flow cytometry with Annexin V-FITC/PI staining, respectively.Results: lncRNA XIST was highly expressed in colorectal cancer tissues and cell lines with the highest expression in HCT-8 cells (P<0.05 or P<0.01). Dual luciferase reporter gene assay validated that lncRNA XIST negatively regulated miR-32-5p (P<0.05),and EZH2 was a target gene of miR-32-5p. Knockdown of lncRNA XIST inhibited proliferation and migration and induced apoptosis of HCT-8 cells (P<0.05 or P<0.01). Further experiments demonstrated that knockdown of lncRNA XIST up-regulated the expression of miR-32-5p and further down-regulated the expression level of EZH2, thereby inhibiting the proliferation and migration of HCT-8 cells and inducing apoptosis. Conclusion: lncRNA XIST promotes proliferation, migration and inhibits apoptosis of HCT-8 cells via miR-32-5p/EZH2 axis.
Objective: To explore the mechanism of lncRNA XIST (XIST) regulating the biological behaviors of colorectal cancer HCT-8 cells via miR-32-5p/EZH2 (enhancer of Zeste homolog 2) axis. Methods: A total of 28 pairs of cancer tissues and corresponding para-cancerous tissues form colorectal cancer patients with complete clinical data were collected from the Colorectal and Anal Surgery,Xiangya Hospital of Central South University during July 2014 and August 2018. The expression levels of lncRNA XIST and miR-32-5p in colorectal cancer tissues and cell lines were detected by qPCR. The targeted relationship between lncRNA XIST, miR-32-5p and EZH2 was verified by dual luciferase reporter gene, and the expression level of EZH2 was further detected by WB. The proliferation,migration and apoptosis of HCT-8 cells were detected by CCK-8, Transwell and flow cytometry with Annexin V-FITC/PI staining, respectively.Results: lncRNA XIST was highly expressed in colorectal cancer tissues and cell lines with the highest expression in HCT-8 cells (P<0.05 or P<0.01). Dual luciferase reporter gene assay validated that lncRNA XIST negatively regulated miR-32-5p (P<0.05),and EZH2 was a target gene of miR-32-5p. Knockdown of lncRNA XIST inhibited proliferation and migration and induced apoptosis of HCT-8 cells (P<0.05 or P<0.01). Further experiments demonstrated that knockdown of lncRNA XIST up-regulated the expression of miR-32-5p and further down-regulated the expression level of EZH2, thereby inhibiting the proliferation and migration of HCT-8 cells and inducing apoptosis. Conclusion: lncRNA XIST promotes proliferation, migration and inhibits apoptosis of HCT-8 cells via miR-32-5p/EZH2 axis.
2019, 26(12):1371-1376.
Abstract:
Objective: To detect the expression of GRHL2 (grainyhead-like-2) in breast cancer tissues and to explore its correlation with clinicopathological characteristics and prognosis of breast cancer (BC) patients，aiming to find new therapeutic target for breast cancer. Method: A total of 88 pairs of BC tissues and corresponding para-cancerous tissues from patients with primary BC that treated and pathologically confirmed at the Second Department of General Surgery, Xinxiang Central Hospital from January 2010 to January 2017 were collected for this study. The expression of GRHL2 in BC tissues and para-cancerous tissues was examined with IHC, and the association between GRHL2 and clinicopathological characteristics of BC patients was analyzed. Moreover, the correlation between GRHL2 and prognosis of BC patients was investigated by analyzing TCGA clinic data for BC. Result: The expression of GRHL2 was significantly higher in BC tissues (75.00%) compared with para-cancerous tissues (36.36%) (P<0.01); Based on the results of GRHL2 expression in 114 cases of normal breast tissues and 1 097 cases of primary breast cancer tissues in TCGA database, the expression of GRHL2 in primary BC tissues was significantly higher than that in normal breast tissues (P<0.01). GRHL2 expression was associated with BC TNM stage, histological grade, HER2 status and lymphnode metastasis status (all P<0.05); TCGA database showed that the RFS of 1 979 BC patients with high GRHL2 expression was significantly shorter than that of the 1 972 cases of BC patients with low GRHL2 expression (HR=1.24, 95%CI:1.11-1.38, P<0.01); GRHL2 expression exerted no significant effect on RFS of TNBC patients or ER+ BC patients (TNBC: HR=1.30，95%CI: 0.89-1.88，P=0.170; ER+ : HR=1.17, 95%CI: 0.76-1.78，P=0.470); however, the RFS of HER2+ BC patients with high GRHL2 expression was significantly shorter than that of HER2+ BC patients with low GRHL2 expression (HR=1.72, 95%CI:1.11-2.68, P=0.015）. Conclusion：Expression level of GRHL2 was up-regulated in BC tissues, and was associated with BC TNM stage, histological grade, HER2 status and the lymphnode metastasis status. GRHL2 plays an important role in the generation and development of BC, indicating poor prognosis.
Objective: To detect the expression of GRHL2 (grainyhead-like-2) in breast cancer tissues and to explore its correlation with clinicopathological characteristics and prognosis of breast cancer (BC) patients，aiming to find new therapeutic target for breast cancer. Method: A total of 88 pairs of BC tissues and corresponding para-cancerous tissues from patients with primary BC that treated and pathologically confirmed at the Second Department of General Surgery, Xinxiang Central Hospital from January 2010 to January 2017 were collected for this study. The expression of GRHL2 in BC tissues and para-cancerous tissues was examined with IHC, and the association between GRHL2 and clinicopathological characteristics of BC patients was analyzed. Moreover, the correlation between GRHL2 and prognosis of BC patients was investigated by analyzing TCGA clinic data for BC. Result: The expression of GRHL2 was significantly higher in BC tissues (75.00%) compared with para-cancerous tissues (36.36%) (P<0.01); Based on the results of GRHL2 expression in 114 cases of normal breast tissues and 1 097 cases of primary breast cancer tissues in TCGA database, the expression of GRHL2 in primary BC tissues was significantly higher than that in normal breast tissues (P<0.01). GRHL2 expression was associated with BC TNM stage, histological grade, HER2 status and lymphnode metastasis status (all P<0.05); TCGA database showed that the RFS of 1 979 BC patients with high GRHL2 expression was significantly shorter than that of the 1 972 cases of BC patients with low GRHL2 expression (HR=1.24, 95%CI:1.11-1.38, P<0.01); GRHL2 expression exerted no significant effect on RFS of TNBC patients or ER+ BC patients (TNBC: HR=1.30，95%CI: 0.89-1.88，P=0.170; ER+ : HR=1.17, 95%CI: 0.76-1.78，P=0.470); however, the RFS of HER2+ BC patients with high GRHL2 expression was significantly shorter than that of HER2+ BC patients with low GRHL2 expression (HR=1.72, 95%CI:1.11-2.68, P=0.015）. Conclusion：Expression level of GRHL2 was up-regulated in BC tissues, and was associated with BC TNM stage, histological grade, HER2 status and the lymphnode metastasis status. GRHL2 plays an important role in the generation and development of BC, indicating poor prognosis.
2019, 26(12):1377-1382.
Abstract:
Objective: To investigate the expression of lncRNA01296 in esophageal cancer (EC) tissues and its effect on the proliferation and migration of EC TE-2 cells. Methods: A total of 36 pairs of esophageal cancer tissues and corresponding para-cancerous tissues were collected from EC patients admitted to the Department of Thoracic Surgery, Affiliated Hospital of Chengde Medical College from January 2017 to September 2018. The human normal esophageal epithelial (HEEC) cells and human esophageal cancer cell lines ECA109, TE-1 and TE-2 were cultured. qPCR was used to detect the mRNA expressions of lincRNA01296, SNRPA (small nuclear ribonucleoprotein A) and NGF (nerve growth factor) in EC tissues and cells. Recombinant lentiviral interference vectoror control vector were used to transfect EC cell lines, as sh-lncRNA01296#1,#2 and Mock groups. WB was used to detect the protein expressions of SNRPA and NGF in transfected cells. MTS assay was used to detect cell proliferation, and Transwell assays were used to detect cell invasion and migration of TE-2 cells after transfection. Results: The mRNA expressions of lncRNA01296, SNRPA and NGF were significantly increased in esophageal cancer tissues and cell lines (all P<0.01), and these expressions in poorly differentiated TE-2 cells were higher than those in highly differentiated ECA109 and TE-1 cells (all P<0.05). The mRNA expressions of lncRNA01296 and NGF in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly lower than those in Mock group (all P<0.01), while the mRNAexpression of SNRPAshowed no statistical difference among three groups (P>0.05). The protein expressions of lncRNA01296 and NGF in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly lower than those in Mock group (all P<0.01). The relative proliferation ability of cells in sh-lncRNA01296#1 and shlncRNA01296# 2 groups was significantly lower than that of Mock group at 48 and 72 h after transfection (P<0.05 or P<0.01). The number of invasive cells was (72.0±6.3), (36.6±4.3) and (33.9±3.7) in Mock, sh-lncRNA01296#1 and sh-lncRNA01296#2 groups, respectively; and the number of migrated cells was (85.2±9.9), (47.5±8.1) and (43.8±6.5), respectively, indicating that the numbers of invasive and migrated cells in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly less than those in Mock group(all P<0.01). Conclusion:lncRNA01296 can up-regulate SNRPA expression to promote NGF-mediated proliferation and metastasis of EC cells, which may provide new target for the diagnosis and treatment of esophagealcancer.
Objective: To investigate the expression of lncRNA01296 in esophageal cancer (EC) tissues and its effect on the proliferation and migration of EC TE-2 cells. Methods: A total of 36 pairs of esophageal cancer tissues and corresponding para-cancerous tissues were collected from EC patients admitted to the Department of Thoracic Surgery, Affiliated Hospital of Chengde Medical College from January 2017 to September 2018. The human normal esophageal epithelial (HEEC) cells and human esophageal cancer cell lines ECA109, TE-1 and TE-2 were cultured. qPCR was used to detect the mRNA expressions of lincRNA01296, SNRPA (small nuclear ribonucleoprotein A) and NGF (nerve growth factor) in EC tissues and cells. Recombinant lentiviral interference vectoror control vector were used to transfect EC cell lines, as sh-lncRNA01296#1,#2 and Mock groups. WB was used to detect the protein expressions of SNRPA and NGF in transfected cells. MTS assay was used to detect cell proliferation, and Transwell assays were used to detect cell invasion and migration of TE-2 cells after transfection. Results: The mRNA expressions of lncRNA01296, SNRPA and NGF were significantly increased in esophageal cancer tissues and cell lines (all P<0.01), and these expressions in poorly differentiated TE-2 cells were higher than those in highly differentiated ECA109 and TE-1 cells (all P<0.05). The mRNA expressions of lncRNA01296 and NGF in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly lower than those in Mock group (all P<0.01), while the mRNAexpression of SNRPAshowed no statistical difference among three groups (P>0.05). The protein expressions of lncRNA01296 and NGF in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly lower than those in Mock group (all P<0.01). The relative proliferation ability of cells in sh-lncRNA01296#1 and shlncRNA01296# 2 groups was significantly lower than that of Mock group at 48 and 72 h after transfection (P<0.05 or P<0.01). The number of invasive cells was (72.0±6.3), (36.6±4.3) and (33.9±3.7) in Mock, sh-lncRNA01296#1 and sh-lncRNA01296#2 groups, respectively; and the number of migrated cells was (85.2±9.9), (47.5±8.1) and (43.8±6.5), respectively, indicating that the numbers of invasive and migrated cells in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly less than those in Mock group(all P<0.01). Conclusion:lncRNA01296 can up-regulate SNRPA expression to promote NGF-mediated proliferation and metastasis of EC cells, which may provide new target for the diagnosis and treatment of esophagealcancer.
2019, 26(12):1383-1386.
Abstract:
Objective: To investigate the expression of CD24 in prostate cancer (PC) tissues, and explore its relationship with clinicopathological features of PC patients. Methods: A total of 40 cases of PC tissues and 36 cases of corresponding para-cacerous tissues resected during surgery at the Department of Urology Surgery, Quanzhou First Hospital Affiliated to Fujian Medical University from February 2016 to March 2019 were collected for this study; in addition, 46 cases of benign prostatic hyperplasia tissues were collected from patients underwent TURP surgery. Flow cytometry was used to detect the expression of CD24 in above mentioned tissues; One-way analysis of variance was used to analyze the relationship between the expression of CD24 and the age, tumor distribution, preoperative serum PSA, postoperative Gleason score, clinical stage and distant metastasis of PC patients. Results: The positive expression rate and MFI (mean fluorensece intensity) value of CD24 in prostate cancer tissues were significantly higher than those in para-cancerous prostate tissues and benign prostatic hyperplasia tissues (all P<0.05); CD24 positive expression rate and MFI value in PC tissues of patients with preoperative serum PSA ≥ 10 ng/ml, postoperative Gleason score ≥8 (low differentiation), clinical stage of T4 and distant metastasis were significantly higher than corresponding control group (all P<0.05); The expression of CD24 gradually increased with the progression of postoperative Gleason score and clinical stage (P<0.05). Conclusions: The expression of CD24 is increased in prostate cancer tissues. The detection of CD24 expression level can help to determine the occurrence, development, invasion and metastasis of prostate cancer, and has potential clinical application value.
Objective: To investigate the expression of CD24 in prostate cancer (PC) tissues, and explore its relationship with clinicopathological features of PC patients. Methods: A total of 40 cases of PC tissues and 36 cases of corresponding para-cacerous tissues resected during surgery at the Department of Urology Surgery, Quanzhou First Hospital Affiliated to Fujian Medical University from February 2016 to March 2019 were collected for this study; in addition, 46 cases of benign prostatic hyperplasia tissues were collected from patients underwent TURP surgery. Flow cytometry was used to detect the expression of CD24 in above mentioned tissues; One-way analysis of variance was used to analyze the relationship between the expression of CD24 and the age, tumor distribution, preoperative serum PSA, postoperative Gleason score, clinical stage and distant metastasis of PC patients. Results: The positive expression rate and MFI (mean fluorensece intensity) value of CD24 in prostate cancer tissues were significantly higher than those in para-cancerous prostate tissues and benign prostatic hyperplasia tissues (all P<0.05); CD24 positive expression rate and MFI value in PC tissues of patients with preoperative serum PSA ≥ 10 ng/ml, postoperative Gleason score ≥8 (low differentiation), clinical stage of T4 and distant metastasis were significantly higher than corresponding control group (all P<0.05); The expression of CD24 gradually increased with the progression of postoperative Gleason score and clinical stage (P<0.05). Conclusions: The expression of CD24 is increased in prostate cancer tissues. The detection of CD24 expression level can help to determine the occurrence, development, invasion and metastasis of prostate cancer, and has potential clinical application value.
2019, 26(12):1387-1391.
Abstract:
调节性T（regulatory T，Treg）细胞是一类控制体内免疫反应性的T细胞亚群，在维持机体的免疫系统稳态和调节免疫应答方面具有重要作用，并且发现在多种肿瘤类型中以较高比例存在，被认为是产生抗肿瘤免疫应答的主要障碍。Treg 细胞在其功能状态和稳定性方面存在异质性，通过多种机制发挥免疫负调控作用，目前在自身免疫和肿瘤免疫的研究中发现，特异性调节不同Treg 细胞群体可改善免疫疗效。但是，如何更加合理有效的以Treg 细胞为靶点抑制肿瘤的进展仍需进一步探索。本文就Treg细胞在肿瘤免疫中的作用机制及治疗应用新策略展开综述。
调节性T（regulatory T，Treg）细胞是一类控制体内免疫反应性的T细胞亚群，在维持机体的免疫系统稳态和调节免疫应答方面具有重要作用，并且发现在多种肿瘤类型中以较高比例存在，被认为是产生抗肿瘤免疫应答的主要障碍。Treg 细胞在其功能状态和稳定性方面存在异质性，通过多种机制发挥免疫负调控作用，目前在自身免疫和肿瘤免疫的研究中发现，特异性调节不同Treg 细胞群体可改善免疫疗效。但是，如何更加合理有效的以Treg 细胞为靶点抑制肿瘤的进展仍需进一步探索。本文就Treg细胞在肿瘤免疫中的作用机制及治疗应用新策略展开综述。
2019, 26(12):1392-1399.
Abstract:
嵌合抗原受体T（chimeric antigen receptor T，CAR-T）细胞是一种通过基因工程表达受体的T细胞，能够识别特定的抗原，是目前最具潜力的靶向肿瘤治疗方法。然而，作为抗癌免疫系统中主要效应细胞之一的CD8+T细胞在肿瘤中发挥作用时，通常处于耗竭状态，而这种功能缺陷的CD8+T细胞是杀伤肿瘤的障碍。肿瘤微环境（tumor microenvironment，TME）中存在许多抑制性因素，例如耗竭性T细胞表面高表达的抑制性受体、免疫抑制细胞群、抑制性因子、转录因素、代谢因素等都对T细胞的分化及耗竭有重要影响。当然，CAR的结构和共刺激域也对CAR-T细胞整体功能发挥着重要作用。本文着重总结近年有关CD8+T细胞耗竭的机制及改善策略的研究进展，为增强CAR-T细胞的抗肿瘤效应提供了潜在思路。
嵌合抗原受体T（chimeric antigen receptor T，CAR-T）细胞是一种通过基因工程表达受体的T细胞，能够识别特定的抗原，是目前最具潜力的靶向肿瘤治疗方法。然而，作为抗癌免疫系统中主要效应细胞之一的CD8+T细胞在肿瘤中发挥作用时，通常处于耗竭状态，而这种功能缺陷的CD8+T细胞是杀伤肿瘤的障碍。肿瘤微环境（tumor microenvironment，TME）中存在许多抑制性因素，例如耗竭性T细胞表面高表达的抑制性受体、免疫抑制细胞群、抑制性因子、转录因素、代谢因素等都对T细胞的分化及耗竭有重要影响。当然，CAR的结构和共刺激域也对CAR-T细胞整体功能发挥着重要作用。本文着重总结近年有关CD8+T细胞耗竭的机制及改善策略的研究进展，为增强CAR-T细胞的抗肿瘤效应提供了潜在思路。
2019, 26(12):1400-1404.
Abstract:
近年来DNA修复途径成为癌症治疗的热门靶点，聚ADP核糖聚合酶［poly（ADP）-ribosepolymerase，PARP]作为DNA修复的关键酶得到了广泛研究，目前上市的PARP抑制剂（PARP inhibitor，PARPi）药物，在乳腺及卵巢等肿瘤中取得了革命性的突破。结直肠癌（CRC）具有异质性，其发生与发展是一个多途径、多基因参与及多步骤的过程，其发病率与病死率在中国逐年上升。研究发现，PARP1 与CRC的发生、发展及治疗密切相关，本文从PARP1 的分子结构及生物学功能、PARPi的作用机制、PARP1在CRC组织中的表达情况、PARP1 与结直肠癌干细胞的关系、PARPi与CRC治疗的关系等5 个方面对PARPi在CRC中作用的研究进展作一系统综述，为临床治疗CRC寻找新的治疗策略。
近年来DNA修复途径成为癌症治疗的热门靶点，聚ADP核糖聚合酶［poly（ADP）-ribosepolymerase，PARP]作为DNA修复的关键酶得到了广泛研究，目前上市的PARP抑制剂（PARP inhibitor，PARPi）药物，在乳腺及卵巢等肿瘤中取得了革命性的突破。结直肠癌（CRC）具有异质性，其发生与发展是一个多途径、多基因参与及多步骤的过程，其发病率与病死率在中国逐年上升。研究发现，PARP1 与CRC的发生、发展及治疗密切相关，本文从PARP1 的分子结构及生物学功能、PARPi的作用机制、PARP1在CRC组织中的表达情况、PARP1 与结直肠癌干细胞的关系、PARPi与CRC治疗的关系等5 个方面对PARPi在CRC中作用的研究进展作一系统综述，为临床治疗CRC寻找新的治疗策略。
2019, 26(12):1405-1409.
Abstract:
以程序性死亡因子1（PD-1）及其配体1（PD-L1）为代表的B7/CD28 家族在肿瘤免疫治疗中显示出极大的应用潜力，但仍有很多PD-L1 检测阴性患者无法从中受益。作为B7 家族成员，人内源性逆转录病毒-H 长末端重复关联蛋白2 (HHLA2)分子结构与PD-L1 等其他B7 家族成员有一定的同源性和相似性，对T细胞有共刺激和共抑制作用，在多数实体肿瘤中呈高表达，且在某些实体肿瘤中表达比PD-L1 更广泛；其通过与受体穿膜和免疫球蛋白结构域2(TMIGD2)结合可促进肿瘤免疫逃逸，导致肿瘤的进展和转移。基于此，HHLA2/TMIGD2 有望成为肿瘤免疫治疗新的通路和靶点之一。本文就HHLA2 及其受体TMIGD2 的分子结构、生物学功能及其在实体肿瘤中作用的研究进展作一综述。
以程序性死亡因子1（PD-1）及其配体1（PD-L1）为代表的B7/CD28 家族在肿瘤免疫治疗中显示出极大的应用潜力，但仍有很多PD-L1 检测阴性患者无法从中受益。作为B7 家族成员，人内源性逆转录病毒-H 长末端重复关联蛋白2 (HHLA2)分子结构与PD-L1 等其他B7 家族成员有一定的同源性和相似性，对T细胞有共刺激和共抑制作用，在多数实体肿瘤中呈高表达，且在某些实体肿瘤中表达比PD-L1 更广泛；其通过与受体穿膜和免疫球蛋白结构域2(TMIGD2)结合可促进肿瘤免疫逃逸，导致肿瘤的进展和转移。基于此，HHLA2/TMIGD2 有望成为肿瘤免疫治疗新的通路和靶点之一。本文就HHLA2 及其受体TMIGD2 的分子结构、生物学功能及其在实体肿瘤中作用的研究进展作一综述。
2019, 26(12):1410-1416.
Abstract:
miR-29b 是最近生物医学界所关注的研究热点之一，尤其在人类癌症中。越来越多的研究发现，miR-29b 在多种癌症中异常表达，与肿瘤细胞增殖、分化、凋亡、侵袭、转移及药物耐受相关，有望成为癌症的新型诊断标志物及治疗靶点。本文重点就miR-29b 在人类癌症中的表达、作用及其调控机制和临床应用的研究进展进行综述，以促进miR-29b 在临床诊断和治疗中的转化应用。
miR-29b 是最近生物医学界所关注的研究热点之一，尤其在人类癌症中。越来越多的研究发现，miR-29b 在多种癌症中异常表达，与肿瘤细胞增殖、分化、凋亡、侵袭、转移及药物耐受相关，有望成为癌症的新型诊断标志物及治疗靶点。本文重点就miR-29b 在人类癌症中的表达、作用及其调控机制和临床应用的研究进展进行综述，以促进miR-29b 在临床诊断和治疗中的转化应用。
联系方式
- 《中国肿瘤生物治疗杂志》
- 1994年创刊
- 主办单位：Chinese Society of Immunology, Chinese Anti-cancer Association
- 邮编：200433
- 电话：021-81871002-22
- 电子邮箱：cjcb@biother.cn
- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
- 国内定价： ￥20元/册
您是第位访问者
Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.
Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.