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Volume 25,Issue 2,2018 Table of Contents
2018, 25(2):109-117.
DOI: 10.3872/j.issn.1007-385X.2018.02.001
Abstract:
MicroRNA (miRNA) is non-coding RNA molecule consisting of 20-25 nucleotides. It plays an important role in regulation of tumorigenesis and progression, including proliferation, differentiation and apoptosis of cancer cells, which directly affect the progress of tumors. Peripheral blood miRNA is relatively more stable, and easier to acquired and detected than tissue miRNA. It is a new generation biomarker for early detection and early diagnosis of tumors. It is also one of the main development directions of research and application in precision medicine. Methods commonly used in peripheral blood miRNA detection are RT- PCR,electrochemical detection, NanoString Technologies, genechip and high-throughput sequencing etc. Multiple miRNAs in peripheral blood are the early diagnostic markers for non-small cell lung cancer, esophageal squamous cell carcinoma, pancreatic cancer, squamous cell carcinoma of the head and neck, ovarian cancer, colorectal cancer, breast cancer, prostate cancer and hematological malignancies. Combined detection of multiple peripheral blood miRNAs, as well as combined detection of tumor-specific miRNAand serological, imaging and other auxiliary methods, can improve the sensitivity and specificity of tumor diagnosis at early stage.
MicroRNA (miRNA) is non-coding RNA molecule consisting of 20-25 nucleotides. It plays an important role in regulation of tumorigenesis and progression, including proliferation, differentiation and apoptosis of cancer cells, which directly affect the progress of tumors. Peripheral blood miRNA is relatively more stable, and easier to acquired and detected than tissue miRNA. It is a new generation biomarker for early detection and early diagnosis of tumors. It is also one of the main development directions of research and application in precision medicine. Methods commonly used in peripheral blood miRNA detection are RT- PCR,electrochemical detection, NanoString Technologies, genechip and high-throughput sequencing etc. Multiple miRNAs in peripheral blood are the early diagnostic markers for non-small cell lung cancer, esophageal squamous cell carcinoma, pancreatic cancer, squamous cell carcinoma of the head and neck, ovarian cancer, colorectal cancer, breast cancer, prostate cancer and hematological malignancies. Combined detection of multiple peripheral blood miRNAs, as well as combined detection of tumor-specific miRNAand serological, imaging and other auxiliary methods, can improve the sensitivity and specificity of tumor diagnosis at early stage.
LIU Fei
,
MENG Lingjiao
,
LIU Shina
,
GU Lina
,
LI Juan
,
ZHANG Jiandong
,
WU Yunyan
,
SANG Meixiang
2018, 25(2):118-124.
DOI: 10.3872/j.issn.1007-385X.2018.02.002
Abstract:
Objective: To investigate the regulating effects of miR-92b on the expression of EZH2 (enhancer of zeste homolog 2) gene and the proliferation and invasion abilities of esophageal cancer (EC) cells. Methods: Fifteen cases of esophageal cancer tissues that preserved in the research center of the Fourth Hospital Affiliated to Heibei Medical University from January 2016 to January 2017 were selected for this study. The bioinformatics tool was used to predict the possible miRNAs that might target EZH2. The mimics of predicted miRNAs were transfected into human esophageal carcinoma cell lines Eca109, respectively. Then the regulation effect of miRNAs on EZH2 gene expression was validated by real-time PCR, Western blotting and dual luciferase reporter experiment. In the meanwhile,EZH2 over-expression plasmids were co-transfected into esophageal carcinoma Eca109 cells, and the effects of miRNAs and EZH2 expression changes on the proliferation, apoptosis , invasion and migration of esophageal carcinoma cells were detected by CCK-8 method,Flow Cytometry, Transwell Invasion and migration assay, respectively. Results: Bioinformatics analysis showed that miR-92b, let-7a and miR-25 could combine with potential binding sites at 3’-terminal non-translation region of EZH2 gene. Real-time PCR results showed that only miR-92b was able to regulate the expression of EZH2, and miR-92b was negatively correlated to EZH2 in esophageal cancer (P<0.01). Compared with mimic-NC, the expression of EZH2 mRNA, protein and luciferase activity in Eca109 cells after miR-92b mimic transfection was significantly down-regulated (both P<0.01). However, miR-92b mimic transfection had no effect on the apoptosis of Eca109 cells. Moreover, the proliferation, invasion and migration of Eca109 cells were significantly inhibited after transfection with miR-92b-mimic (P<0.01). In addition, after co-transfection with EZH2 over-expression plasmids, the effects of miR-92b-mimic on the proliferation, invasion and migration of Eca109 cells were significantly weakened (P<0.01). Conclusion: miR-92b can inhibit the proliferation, invasion and migration of esophageal carcinoma cells, and its mechanism may be related to its target regulation ofEZH2.
Objective: To investigate the regulating effects of miR-92b on the expression of EZH2 (enhancer of zeste homolog 2) gene and the proliferation and invasion abilities of esophageal cancer (EC) cells. Methods: Fifteen cases of esophageal cancer tissues that preserved in the research center of the Fourth Hospital Affiliated to Heibei Medical University from January 2016 to January 2017 were selected for this study. The bioinformatics tool was used to predict the possible miRNAs that might target EZH2. The mimics of predicted miRNAs were transfected into human esophageal carcinoma cell lines Eca109, respectively. Then the regulation effect of miRNAs on EZH2 gene expression was validated by real-time PCR, Western blotting and dual luciferase reporter experiment. In the meanwhile,EZH2 over-expression plasmids were co-transfected into esophageal carcinoma Eca109 cells, and the effects of miRNAs and EZH2 expression changes on the proliferation, apoptosis , invasion and migration of esophageal carcinoma cells were detected by CCK-8 method,Flow Cytometry, Transwell Invasion and migration assay, respectively. Results: Bioinformatics analysis showed that miR-92b, let-7a and miR-25 could combine with potential binding sites at 3’-terminal non-translation region of EZH2 gene. Real-time PCR results showed that only miR-92b was able to regulate the expression of EZH2, and miR-92b was negatively correlated to EZH2 in esophageal cancer (P<0.01). Compared with mimic-NC, the expression of EZH2 mRNA, protein and luciferase activity in Eca109 cells after miR-92b mimic transfection was significantly down-regulated (both P<0.01). However, miR-92b mimic transfection had no effect on the apoptosis of Eca109 cells. Moreover, the proliferation, invasion and migration of Eca109 cells were significantly inhibited after transfection with miR-92b-mimic (P<0.01). In addition, after co-transfection with EZH2 over-expression plasmids, the effects of miR-92b-mimic on the proliferation, invasion and migration of Eca109 cells were significantly weakened (P<0.01). Conclusion: miR-92b can inhibit the proliferation, invasion and migration of esophageal carcinoma cells, and its mechanism may be related to its target regulation ofEZH2.
2018, 25(2):125-131.
DOI: 10.3872/j.issn.1007-385X.2018.02.003
Abstract:
Objective: To investigate the effects of FPR1 (formyl peptide receptor 1) antagonist Boc2 on migration, invasion, proliferation and tumorigenicity of human lung adenocarcinoma cells under hypoxia conditions. Methods: The protein expressions of hypoxia inducible factor 1α (HIF-1α) and FPR1 in human lung adenocarcinoma A549 cells induced by hypoxia was detected by Western blotting.FPR1 antagonist Boc2 was used to treat the hypoxia-induced A549 cells in vitro. The cells were divided into three groups: control group (cultured under normoxic condition), hypoxia group and hypoxia+Boc2 treatment group. Cell scratch test, transwell matrigel invasion assay and MTT method were used to detect the migration, invasion and proliferation of each group of cells, respectively. The A549 cells of each group were inoculated into nude mice to prepare xenograft model. After 4 weeks, the nude mice were sacrificed, and the differences in average tumor volume and mass, tumor formation rate, the expression of migration-related protein-E-cadherin (E-cad)and invasion-related protein-matrix metalloproteinase 9 (MMP-9) were analyzed. Results: Hypoxia induction can promote the expression of FPR1 protein in A549 cells in a time-dependent manner (P<0.05). The results of cell experiments showed that the ability of migration,invasion and proliferation of cells in hypoxia group were significantly higher than those in control group (P<0.01); while compared with hypoxia group, Boc2 treatment significantly inhibited the migration, invasion and proliferation of A549 cells (P<0.05). The results of nude mice experiments showed that the average volume and mass of nude mice in hypoxia group were significantly higher than those in the control group (all P<0.01). But the mean volume and mass of nude mice in hypoxia+Boc2 treatment group were significantly lower than those in the hypoxia group (all P<0.01). The rate of tumor formation in nude mice of hypoxia group was 100.0% (15/15), which was significantly higher than 60.0% (9/15) in the control group (χ2=7.500, P=0.006) and 73.3% (11/15) in the hypoxia +Boc2 treatment group (χ2=4.615, P=0.032). The expression of E-cad and MMP-9 protein in hypoxia group was significantly higher than that in control group (P<0.01), while Boc2 treatment significantly decreased the expression of E-cad and MMP-9 protein in hypoxia group (P<0.05). Conclusions: FPR1 antagonist Boc2 can significantly inhibit the migration, invasion, proliferation and tumorigenicity of hypoxia-induced human lung adenocarcinoma A549 cells, indicating that FPR1 plays an important role in the development and progression of human lung adenocarcinoma and may become a potential target of human lung adenocarcinoma treatment.
Objective: To investigate the effects of FPR1 (formyl peptide receptor 1) antagonist Boc2 on migration, invasion, proliferation and tumorigenicity of human lung adenocarcinoma cells under hypoxia conditions. Methods: The protein expressions of hypoxia inducible factor 1α (HIF-1α) and FPR1 in human lung adenocarcinoma A549 cells induced by hypoxia was detected by Western blotting.FPR1 antagonist Boc2 was used to treat the hypoxia-induced A549 cells in vitro. The cells were divided into three groups: control group (cultured under normoxic condition), hypoxia group and hypoxia+Boc2 treatment group. Cell scratch test, transwell matrigel invasion assay and MTT method were used to detect the migration, invasion and proliferation of each group of cells, respectively. The A549 cells of each group were inoculated into nude mice to prepare xenograft model. After 4 weeks, the nude mice were sacrificed, and the differences in average tumor volume and mass, tumor formation rate, the expression of migration-related protein-E-cadherin (E-cad)and invasion-related protein-matrix metalloproteinase 9 (MMP-9) were analyzed. Results: Hypoxia induction can promote the expression of FPR1 protein in A549 cells in a time-dependent manner (P<0.05). The results of cell experiments showed that the ability of migration,invasion and proliferation of cells in hypoxia group were significantly higher than those in control group (P<0.01); while compared with hypoxia group, Boc2 treatment significantly inhibited the migration, invasion and proliferation of A549 cells (P<0.05). The results of nude mice experiments showed that the average volume and mass of nude mice in hypoxia group were significantly higher than those in the control group (all P<0.01). But the mean volume and mass of nude mice in hypoxia+Boc2 treatment group were significantly lower than those in the hypoxia group (all P<0.01). The rate of tumor formation in nude mice of hypoxia group was 100.0% (15/15), which was significantly higher than 60.0% (9/15) in the control group (χ2=7.500, P=0.006) and 73.3% (11/15) in the hypoxia +Boc2 treatment group (χ2=4.615, P=0.032). The expression of E-cad and MMP-9 protein in hypoxia group was significantly higher than that in control group (P<0.01), while Boc2 treatment significantly decreased the expression of E-cad and MMP-9 protein in hypoxia group (P<0.05). Conclusions: FPR1 antagonist Boc2 can significantly inhibit the migration, invasion, proliferation and tumorigenicity of hypoxia-induced human lung adenocarcinoma A549 cells, indicating that FPR1 plays an important role in the development and progression of human lung adenocarcinoma and may become a potential target of human lung adenocarcinoma treatment.
2018, 25(2):132-136.
DOI: 10.3872/j.issn.1007-385X.2018.02.004
Abstract:
Objective: To construct recombinant plasmid Egr1-XPO4 and evaluate its synergic inhibition with 5-FU against hepatocarcinoma SK-Hep1 cells. Methods: The XPO4 gene was inserted into vector carrying promoter Egr1 to construct a new recombinant vector,Egr1-XPO4, which was then transfected into human hepatocarcinoma cell line SK-Hep1 and sensitized with chemotherapeutic drug 5-FU. Western blotting was adopted to examine the protein expression of XPO4; CCK assay was used to detect SK-Hep1 cell proliferation after transfection, and Flow Cytometry with Annexin V-FITC/PI staining was used to detect the apoptosis of SK-Hep1 cells. SKHep1 cell xenograft model was constructed on nude mice, and the effect of Egr1-XPO4 in combination with 5-FU on the growth of xenograft was observed. Results: The recombinant plasmid Egr1-XPO4 was successfully constructed.With the sensitization of 5-FU, the expression of XPO4 protein in SK-Hep1 cells was significantly elevated after Egr1-XPO4 transfection, and the evlevation was in a 5-FU dose- depend manner.The combined treatment of Egr1-XPO4 and 5-FU produced a significantly stronger inhibition against SKHep1 cell proliferation and greatly promoted apoptosis of SK-Hep1cells compared with 5-FU or pEgr-XPO4 mono-treatment group (all P<0.05). And in vivo antitumor experiment showed that the tumor volume in Egr1-XPO4+5-FU treatment group was significantly smaller than that of Egr1-XPO4 or 5-FU mono-treatment group (P<0.05). Conclusion: The recombinant plasmid Egr1-XPO4 in combination with 5-FU could exertsynergic inhibitionagainst hepatocarcinomaSK-Hep1 cells.
Objective: To construct recombinant plasmid Egr1-XPO4 and evaluate its synergic inhibition with 5-FU against hepatocarcinoma SK-Hep1 cells. Methods: The XPO4 gene was inserted into vector carrying promoter Egr1 to construct a new recombinant vector,Egr1-XPO4, which was then transfected into human hepatocarcinoma cell line SK-Hep1 and sensitized with chemotherapeutic drug 5-FU. Western blotting was adopted to examine the protein expression of XPO4; CCK assay was used to detect SK-Hep1 cell proliferation after transfection, and Flow Cytometry with Annexin V-FITC/PI staining was used to detect the apoptosis of SK-Hep1 cells. SKHep1 cell xenograft model was constructed on nude mice, and the effect of Egr1-XPO4 in combination with 5-FU on the growth of xenograft was observed. Results: The recombinant plasmid Egr1-XPO4 was successfully constructed.With the sensitization of 5-FU, the expression of XPO4 protein in SK-Hep1 cells was significantly elevated after Egr1-XPO4 transfection, and the evlevation was in a 5-FU dose- depend manner.The combined treatment of Egr1-XPO4 and 5-FU produced a significantly stronger inhibition against SKHep1 cell proliferation and greatly promoted apoptosis of SK-Hep1cells compared with 5-FU or pEgr-XPO4 mono-treatment group (all P<0.05). And in vivo antitumor experiment showed that the tumor volume in Egr1-XPO4+5-FU treatment group was significantly smaller than that of Egr1-XPO4 or 5-FU mono-treatment group (P<0.05). Conclusion: The recombinant plasmid Egr1-XPO4 in combination with 5-FU could exertsynergic inhibitionagainst hepatocarcinomaSK-Hep1 cells.
5 Effect of curcumin on angiogenesis of rats with DEN-induced hepatocellular carcinoma under hypoxia
2018, 25(2):137-141.
DOI: 10.3872/j.issn.1007-385X.2018.02.005
Abstract:
Objective: To investigate the effect of curcumin on angiogenesis in rats with DEN (diethylnitrosamine)-induced HCC (hepatocellular carcinoma) under hypoxia. Methods: Rat HCC was induced by DEN, and its hepatic hypoxia model was established by ligating hepatic artery. The rats with established HCC model were randomly divided into four groups according to digital table method: lipiodol embolization group (group A), lipiodol combined with curcumin embolization group (group B), lipiodol combined with peripheral liver capsule group (group C), lipiodol combined with curcumin and peripheral liver capsule group (group D), with 10 rats in each group. VEGF expression in HCC cells and tissues, microvessel density (MVD), and median survival time (MST) of rats in each group were compared. Results: VEGF protein expression and microvessel density in group B, D were significantly lower than those in A group (P<0.01), while those in C group had no significant difference compared with group A (P >0.05). MST in group B, C and D was significantly longer than that in group A (P<0.05), and the MST in group D was higher than that in group B and C (P<0.05). Conclusion:Curcumin can inhibit tumor angiogenesis and decrease VEGF expression and MVD in HCC rats under hypoxia, thus further prolong the survival time of the rats.
Objective: To investigate the effect of curcumin on angiogenesis in rats with DEN (diethylnitrosamine)-induced HCC (hepatocellular carcinoma) under hypoxia. Methods: Rat HCC was induced by DEN, and its hepatic hypoxia model was established by ligating hepatic artery. The rats with established HCC model were randomly divided into four groups according to digital table method: lipiodol embolization group (group A), lipiodol combined with curcumin embolization group (group B), lipiodol combined with peripheral liver capsule group (group C), lipiodol combined with curcumin and peripheral liver capsule group (group D), with 10 rats in each group. VEGF expression in HCC cells and tissues, microvessel density (MVD), and median survival time (MST) of rats in each group were compared. Results: VEGF protein expression and microvessel density in group B, D were significantly lower than those in A group (P<0.01), while those in C group had no significant difference compared with group A (P >0.05). MST in group B, C and D was significantly longer than that in group A (P<0.05), and the MST in group D was higher than that in group B and C (P<0.05). Conclusion:Curcumin can inhibit tumor angiogenesis and decrease VEGF expression and MVD in HCC rats under hypoxia, thus further prolong the survival time of the rats.
2018, 25(2):142-147.
DOI: 10.3872/j.issn.1007-385X.2018.02.006
Abstract:
Objective: To investigate the effects of interleukin-18 over-expression on the in vitro and in vivo proliferation of human colorectal cancer (CRC) HCT-116 cells. Methods: A recombinant lentivirus vector containing human IL-18 gene fragment was constructed.Then theCRC HCT-116 cell line stably expressing human IL-18 (HCT-116/IL-18) was obtained by recombinant lentivirus transfection. In vitro proliferation of HCT-116/IL-18 cells and wild-type HCT-116 cells was determined by CCK-8 method. The expressions of IL-18, Cyclin D1, proliferating cell nuclear antigen (PCNA) and DNA damage repair enzyme (PARP) were detected by Western blotting. HCT-116 and HCT-116/IL-18 cells were inoculated into left and right axillas of Balb/c nude mice, respectively. Then the tumorigenicity and the growth of transplanted tumor were observed. The expressions of IL-18 and PCNA in xenograft tissues were detected by immunohistochemistry analysis. Results: IL-18 gene over-expression in HCT-116 cells could delay the proliferation of HCT-116 cells (P<0.05 or P<0.01). PARP expression was increased significantly and PCNA, Cyclin D1 expression were decreased in HCT-116/IL-18 cells as compared to that of HCT-116 cells (P<0.01).The tumorigenicity of HCT-116/IL-18 cell was significantly decreased in nude mice with a tumor-formation rate of 43%; Compared with control group, HCT-116/IL-18cell line had a longer tumorigensis time,slower growth and smaller tumor volume; moreover, PCNA protein expression was down-regulated in HCT-116/IL-18 xenograft tissue-sas shown by immunohistochemistry analysis (P<0.01). Conclusion: IL-18 over-expression inhibited the growth and proliferation of HCT-116cells both in vitro andin vivo, and the mechanism might be related with IL-18 regulating cell cycle and promotingDNAdamage.
Objective: To investigate the effects of interleukin-18 over-expression on the in vitro and in vivo proliferation of human colorectal cancer (CRC) HCT-116 cells. Methods: A recombinant lentivirus vector containing human IL-18 gene fragment was constructed.Then theCRC HCT-116 cell line stably expressing human IL-18 (HCT-116/IL-18) was obtained by recombinant lentivirus transfection. In vitro proliferation of HCT-116/IL-18 cells and wild-type HCT-116 cells was determined by CCK-8 method. The expressions of IL-18, Cyclin D1, proliferating cell nuclear antigen (PCNA) and DNA damage repair enzyme (PARP) were detected by Western blotting. HCT-116 and HCT-116/IL-18 cells were inoculated into left and right axillas of Balb/c nude mice, respectively. Then the tumorigenicity and the growth of transplanted tumor were observed. The expressions of IL-18 and PCNA in xenograft tissues were detected by immunohistochemistry analysis. Results: IL-18 gene over-expression in HCT-116 cells could delay the proliferation of HCT-116 cells (P<0.05 or P<0.01). PARP expression was increased significantly and PCNA, Cyclin D1 expression were decreased in HCT-116/IL-18 cells as compared to that of HCT-116 cells (P<0.01).The tumorigenicity of HCT-116/IL-18 cell was significantly decreased in nude mice with a tumor-formation rate of 43%; Compared with control group, HCT-116/IL-18cell line had a longer tumorigensis time,slower growth and smaller tumor volume; moreover, PCNA protein expression was down-regulated in HCT-116/IL-18 xenograft tissue-sas shown by immunohistochemistry analysis (P<0.01). Conclusion: IL-18 over-expression inhibited the growth and proliferation of HCT-116cells both in vitro andin vivo, and the mechanism might be related with IL-18 regulating cell cycle and promotingDNAdamage.
2018, 25(2):148-152.
DOI: 10.3872/j.issn.1007-385X.2018.02.007
Abstract:
Objective: To investigate the osteogenic differentiation characteristics of mesenchymal stem cell (MSC) derived from bone marrow in patients with myelodysplastic syndromes (MDS) and its clinical significance. Methods: Bone marrow samples from 30 cases of newly diagnosed untreated MDS patient at Affiliated Hospital of Heibei University were collected for this study. MSCs from MDS patients and normal subjects were isolated and cultured, and morphological characteristics of MSCs were observed in vitro; under proper conditions, MSCs were induced to differentiate into osteoblasts and adipocytes; The formation of calcium nodules at 14th day after osteogenic differentiation was observed by alizarin red staining; mRNA expressions of osteogenic differentiation transcription factors Ostefix and RUNX2 in undifferentiated MSCs, as well as the mRNA expression of Jagged-1, which involved in the transformation from hematopoietic cells into leukemic cells, were detected by quantitative PCR. Results: The MSCs derived from patients with MDS were characterized with increased cell volume and decreased differentiation potential. Compared with the control group, the expression levels of osteogenic differentiation transcription factors Osterix and RUNX2 were significantly decreased (P < 0.05). Alizarin red staining showed that the content of calcium nodules in MDS group was significantly less than that in the normal control group, while the expression level of Jagged-1 was significantly higher (P < 0.05). Conclusion: MSCs derived from bone marrow of MDS patients showed significant increased cell volume, decreased differentiation potential and elevated Jagged-1 expression; all of these might play important roles in the .hematopoietic failure and progression to acute myeloid leukemia in MDS patients.
Objective: To investigate the osteogenic differentiation characteristics of mesenchymal stem cell (MSC) derived from bone marrow in patients with myelodysplastic syndromes (MDS) and its clinical significance. Methods: Bone marrow samples from 30 cases of newly diagnosed untreated MDS patient at Affiliated Hospital of Heibei University were collected for this study. MSCs from MDS patients and normal subjects were isolated and cultured, and morphological characteristics of MSCs were observed in vitro; under proper conditions, MSCs were induced to differentiate into osteoblasts and adipocytes; The formation of calcium nodules at 14th day after osteogenic differentiation was observed by alizarin red staining; mRNA expressions of osteogenic differentiation transcription factors Ostefix and RUNX2 in undifferentiated MSCs, as well as the mRNA expression of Jagged-1, which involved in the transformation from hematopoietic cells into leukemic cells, were detected by quantitative PCR. Results: The MSCs derived from patients with MDS were characterized with increased cell volume and decreased differentiation potential. Compared with the control group, the expression levels of osteogenic differentiation transcription factors Osterix and RUNX2 were significantly decreased (P < 0.05). Alizarin red staining showed that the content of calcium nodules in MDS group was significantly less than that in the normal control group, while the expression level of Jagged-1 was significantly higher (P < 0.05). Conclusion: MSCs derived from bone marrow of MDS patients showed significant increased cell volume, decreased differentiation potential and elevated Jagged-1 expression; all of these might play important roles in the .hematopoietic failure and progression to acute myeloid leukemia in MDS patients.
2018, 25(2):153-157.
DOI: 10.3872/j.issn.1007-385X.2018.02.008
Abstract:
Objective: To investigate the effects of plasma-cytoma variant translocation gene 1 (PVT1) on proliferation, migration and invasion of ovarian cancer SKOV3 cells. Methods: Quantitative reverse transcription PCR (qRT-PCR) was used to detect the expression of PVT1 in 32 pairs of ovarian cancer tissues and corresponding para-carcinoma tissues. The effects of PVT1 on proliferation, migration and invasion of ovarian cancer cells were studied by CCK-8, scratch wound healing assay and Transwell assay. Results: The expression level of PVT1 in SKOV3 cells and ovarian cancer tissues was significantly increased (all P<0.01). The expression level of PVT1 was correlated with histological grade, FIGO stage and lymph node metastasis in patients with ovarian cancer (P<0.05 or P<0.01). After transfection with PVT1 siRNA for 36, 48 h, expression of PVT1 was significantly decreased in SKOV3 cells; and the inhibition of PVT1 expression could decrease the proliferation ability and inhibit the migration and invasion of SKOV3 cells (P<0.05 or 0.01). Conclusion: LncRNA PVT1 was highly expressed in ovarian cancer. Down-regulation of PVT1 could inhibit the proliferation,migration and invasion of ovarian cancer SKOV3 cells.
Objective: To investigate the effects of plasma-cytoma variant translocation gene 1 (PVT1) on proliferation, migration and invasion of ovarian cancer SKOV3 cells. Methods: Quantitative reverse transcription PCR (qRT-PCR) was used to detect the expression of PVT1 in 32 pairs of ovarian cancer tissues and corresponding para-carcinoma tissues. The effects of PVT1 on proliferation, migration and invasion of ovarian cancer cells were studied by CCK-8, scratch wound healing assay and Transwell assay. Results: The expression level of PVT1 in SKOV3 cells and ovarian cancer tissues was significantly increased (all P<0.01). The expression level of PVT1 was correlated with histological grade, FIGO stage and lymph node metastasis in patients with ovarian cancer (P<0.05 or P<0.01). After transfection with PVT1 siRNA for 36, 48 h, expression of PVT1 was significantly decreased in SKOV3 cells; and the inhibition of PVT1 expression could decrease the proliferation ability and inhibit the migration and invasion of SKOV3 cells (P<0.05 or 0.01). Conclusion: LncRNA PVT1 was highly expressed in ovarian cancer. Down-regulation of PVT1 could inhibit the proliferation,migration and invasion of ovarian cancer SKOV3 cells.
2018, 25(2):158-162.
DOI: 10.3872/j.issn.1007-385X.2018.02.009
Abstract:
Objective: To investigate the expression of long non-coding RNA LINC01001 in breast cancer tissues and its effect on the proliferation of breast cancer MCF-7 cells. Methods: The expression levels of lncRNA LINC01001 were analyzed in 12 cases of cancer and para-cancer tissues from breast cancer patients, who underwent surgical resection in Affiliated People’s Hospital of Hubei University of Medicine from March 2016 to June 2017. The plasmid over-expressing LINC01001 was transfected into human breast cancer MCF-7 cells. The cell cycle distribution and proliferation ability of MCF-7 cells were detected by flow cytometry and MTT assay, respectively. The mRNA expressions of miR-485-5p and CDKN1A mRNA were detected by qRT-PCR, and the protein expressions of CDKN1A, CDK4, CDK6 and Cyclin D1 were detected by Western blotting. Results: The expression level of lncRNA LINC01001 in breast cancer tissues was lower than that in para-cancer tissues (P<0.01). LINC01001 recombinant plasmid transfection significantly inhibited cell cycle progression (P<0.05) and cell proliferation (P<0.05) of MCF-7 cells. qRT-PCR showed that the expression level of miR-485-5p was decreased (P<0.01) and the expression level of CDKN1A mRNA was increased (P<0.01) after over-expressing LINC01001. Western blot results confirmed that over-expression of LINC01001 could promote the expression of CDKN1A protein, but decrease the expressions of CDK4, CDK6 and Cyclin D1 proteins. Conclusion: The expression of LINC01001 in breast cancer tissues was decreased. LINC01001 may down-regulate the expression of miR-485-5p to up-regulate the expression of CDKN1A, and further to inhibit the proliferation of breast cancer MCF-7 cells, providing experimental basis for the clinical application of lncRNA.
Objective: To investigate the expression of long non-coding RNA LINC01001 in breast cancer tissues and its effect on the proliferation of breast cancer MCF-7 cells. Methods: The expression levels of lncRNA LINC01001 were analyzed in 12 cases of cancer and para-cancer tissues from breast cancer patients, who underwent surgical resection in Affiliated People’s Hospital of Hubei University of Medicine from March 2016 to June 2017. The plasmid over-expressing LINC01001 was transfected into human breast cancer MCF-7 cells. The cell cycle distribution and proliferation ability of MCF-7 cells were detected by flow cytometry and MTT assay, respectively. The mRNA expressions of miR-485-5p and CDKN1A mRNA were detected by qRT-PCR, and the protein expressions of CDKN1A, CDK4, CDK6 and Cyclin D1 were detected by Western blotting. Results: The expression level of lncRNA LINC01001 in breast cancer tissues was lower than that in para-cancer tissues (P<0.01). LINC01001 recombinant plasmid transfection significantly inhibited cell cycle progression (P<0.05) and cell proliferation (P<0.05) of MCF-7 cells. qRT-PCR showed that the expression level of miR-485-5p was decreased (P<0.01) and the expression level of CDKN1A mRNA was increased (P<0.01) after over-expressing LINC01001. Western blot results confirmed that over-expression of LINC01001 could promote the expression of CDKN1A protein, but decrease the expressions of CDK4, CDK6 and Cyclin D1 proteins. Conclusion: The expression of LINC01001 in breast cancer tissues was decreased. LINC01001 may down-regulate the expression of miR-485-5p to up-regulate the expression of CDKN1A, and further to inhibit the proliferation of breast cancer MCF-7 cells, providing experimental basis for the clinical application of lncRNA.
2018, 25(2):163-169.
DOI: 10.3872/j.issn.1007-385X.2018.02.010
Abstract:
Objective: To search valuable candidate molecular markers for LSCC by screening and identifying differentially expressed long non-coding RNAs (lncRNAs) in metastatic laryngeal squamous cell carcinoma (LSCC) with high throughput gene microarray technique.Methods: Four pairs of LSCC tissues and corresponding para-cancer tissues that pathologically confirmed with lymph node metastasis were collected from Bio-sample lab of Otorhinolaryngology Department, the Second Hospital of Hebei Medical University. After total RNA extraction, the SBC-lncRNA (human 4x180k) chip assay was then applied to detect the differentially expressed lncRNAs and mRNAs, and Fold-change and Student's t-test methods were used to identify differentially expressed genes; the Fold Change (linear)≤0.5 or ≥2.0, P<0.05 was used to identify the differentially expressed genes. The reliability of the chip results was confirmed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results: The gene expression profiles of metastatic LSCC tissues and corresponding para-cancer tissues were significantly different. There were 3 073 differentially expressed lncRNAs, including 1 967 up-regulated and 1 106 down-regulated lncRNAs in cancer tissues. There were 2 809 differentially expressed mRNAs, including 1 791 up- regulated and 1 018 down-regulated mRNAs in cancer tissues. The differentially expressed lncRNAs were mainly in-volved in cell proliferation and apoptosis, immune response biological process, and were associated with cytokine and cytokine receptor interaction, chemokine signaling pathway, cell cycle regulation, P53 signaling pathway, etc. In addition, 10 significantly differentially expressed lncRNAs were chosen and validated by qRT-PCR in 25 cases of LSCC tissues, and the results were in agree with microarray detection. Conclusions: There were obvious differences in lncRNAs expression between metastasis LSCC and corresponding paracancer tissues; in-depth analysis of these differences may has important significance on clarifying the mechanisms of invasion and metastasis of LSCC, which can provide the theoretical basis for biomarker screening and effective targeted therapy for LSCC.
Objective: To search valuable candidate molecular markers for LSCC by screening and identifying differentially expressed long non-coding RNAs (lncRNAs) in metastatic laryngeal squamous cell carcinoma (LSCC) with high throughput gene microarray technique.Methods: Four pairs of LSCC tissues and corresponding para-cancer tissues that pathologically confirmed with lymph node metastasis were collected from Bio-sample lab of Otorhinolaryngology Department, the Second Hospital of Hebei Medical University. After total RNA extraction, the SBC-lncRNA (human 4x180k) chip assay was then applied to detect the differentially expressed lncRNAs and mRNAs, and Fold-change and Student's t-test methods were used to identify differentially expressed genes; the Fold Change (linear)≤0.5 or ≥2.0, P<0.05 was used to identify the differentially expressed genes. The reliability of the chip results was confirmed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results: The gene expression profiles of metastatic LSCC tissues and corresponding para-cancer tissues were significantly different. There were 3 073 differentially expressed lncRNAs, including 1 967 up-regulated and 1 106 down-regulated lncRNAs in cancer tissues. There were 2 809 differentially expressed mRNAs, including 1 791 up- regulated and 1 018 down-regulated mRNAs in cancer tissues. The differentially expressed lncRNAs were mainly in-volved in cell proliferation and apoptosis, immune response biological process, and were associated with cytokine and cytokine receptor interaction, chemokine signaling pathway, cell cycle regulation, P53 signaling pathway, etc. In addition, 10 significantly differentially expressed lncRNAs were chosen and validated by qRT-PCR in 25 cases of LSCC tissues, and the results were in agree with microarray detection. Conclusions: There were obvious differences in lncRNAs expression between metastasis LSCC and corresponding paracancer tissues; in-depth analysis of these differences may has important significance on clarifying the mechanisms of invasion and metastasis of LSCC, which can provide the theoretical basis for biomarker screening and effective targeted therapy for LSCC.
2018, 25(2):170-176.
DOI: 10.3872/j.issn.1007-385X.2018.02.011
Abstract:
Objective: To investigate the expression and clinical significance of PD-1/PD-L1 in gastric cancer (GC) tissues. Methods:Paraffin embedded tumor tissues and clinical data of 82 GC patients who had undergone operation at the Fourth Hospital of Hebei Medical University from January 2007 to December 2007 were collected, and their survival status was followed. The protein expressions of PD-1 and PD-L1 in tumor tissues were detected by immunohistochemistry. Kaplan-Meier analysis and Log-Rank test were adopted to analyze the survival of GC patients, and the ROC curve was plotted. Results: The positive rate of PD- L1 protein expression was 42.68% while the positive rate of PD-1 expression was 13.41% in GC tissues. The positive rate of PD-1 and PD-L1 expression in GC tissues of patients without pre-operative distant metastasis was significantly lower than those patients with pre-operative metastasis (PD-1：3.28% vs 42.86%; PD-L1：13.11% vs 90.48%; all P<0.01). The positive rate of PD-L1 expression in tumor stroma of patients without pre-operative distant metastasis was significantly lower than those with metastasis (PD-L1: 13.11% vs 47.62%, P<0.01). The resection range of stomach, PD-L1 over-expression and the presence of pre-operative distant metastasis were the adverse factors affecting the prognosis of patients with GC (P<0.05). Conclusion: PD-1 and PD-L1 expressions in GC tissues were closely related to the presence of pre-operative distant metastasis and the depth of tumor infiltration. The postoperative survival of patients who were PD-L1 positive was shorter than the negative ones.
Objective: To investigate the expression and clinical significance of PD-1/PD-L1 in gastric cancer (GC) tissues. Methods:Paraffin embedded tumor tissues and clinical data of 82 GC patients who had undergone operation at the Fourth Hospital of Hebei Medical University from January 2007 to December 2007 were collected, and their survival status was followed. The protein expressions of PD-1 and PD-L1 in tumor tissues were detected by immunohistochemistry. Kaplan-Meier analysis and Log-Rank test were adopted to analyze the survival of GC patients, and the ROC curve was plotted. Results: The positive rate of PD- L1 protein expression was 42.68% while the positive rate of PD-1 expression was 13.41% in GC tissues. The positive rate of PD-1 and PD-L1 expression in GC tissues of patients without pre-operative distant metastasis was significantly lower than those patients with pre-operative metastasis (PD-1：3.28% vs 42.86%; PD-L1：13.11% vs 90.48%; all P<0.01). The positive rate of PD-L1 expression in tumor stroma of patients without pre-operative distant metastasis was significantly lower than those with metastasis (PD-L1: 13.11% vs 47.62%, P<0.01). The resection range of stomach, PD-L1 over-expression and the presence of pre-operative distant metastasis were the adverse factors affecting the prognosis of patients with GC (P<0.05). Conclusion: PD-1 and PD-L1 expressions in GC tissues were closely related to the presence of pre-operative distant metastasis and the depth of tumor infiltration. The postoperative survival of patients who were PD-L1 positive was shorter than the negative ones.
2018, 25(2):177-181.
DOI: 10.3872/j.issn.1007-385X.2018.02.012
Abstract:
Objective: To investigate the relationship between expression of MICA/B (MHC class I chain-related protein A/B) and disease-free survival (DFS) of patients with HER2+ (human epidermal growth factor receptor 2) breast cancer tissue. Methods: Twenty six cases of corresponding para-cancerous tissue and 100 cases of HER2+ breast cancer tissue that preserved in wax at Zhengzhou People’s Hospital Affiliated to Southern Medical University from January 2009 to June 2010 were collected for this study. Expression of MICA/B in these tissue samples was detected by immunohistochemistry; and the relationship between MICA/B expression with clinicopathologic features as well as DFS was analyzed with Kaplan-Meier survival curve. Results: The expression of MICA/B in adjacent paracancerous tissues was negative (0/26), however, it was highly positive in cancer tissues (92/100), and the percentage with high expression was 65%(65/100), the difference was significant (P<0.05). High MICA/B expression rate in stage I was significantly higher than that in stage Ⅱ-Ⅲ (77.55% vs 52.94%，P<0.05), and the high expression rate in stage T1 was also significantly higher than that in stage T2-T4 (75.00% vs 52.27%，P<0.05). High MICA/B expression rate in ER+, PR+ group (with positive number ≥1%) was significantly lower than that in ER- , PR- group (ER：52.38% vs 74.14%，PR：51.35% vs 73.02%，all P<0.05). MICA/B expression was correlated with clinical stages, the expression of ER, PR and tumor size (all P<0.05), but not associated with menopausal status, histological grade and lymph node metastasis (all P>0.05). Over-expression of MICA/B was closely associated with much better 6-year DFS rate in patients no matter with or without targeted therapy (the targeted group: 90.6% vs 72.2%; the untargeted group: 78.4% vs 58.8%, all P<0.05). Conclusion: Over-expression of MICA/B in HER2+ breast cancer tissue is closely related to DFS, which may be served as a potential prognosis indicator for patients with HER2+ breast cancer.
Objective: To investigate the relationship between expression of MICA/B (MHC class I chain-related protein A/B) and disease-free survival (DFS) of patients with HER2+ (human epidermal growth factor receptor 2) breast cancer tissue. Methods: Twenty six cases of corresponding para-cancerous tissue and 100 cases of HER2+ breast cancer tissue that preserved in wax at Zhengzhou People’s Hospital Affiliated to Southern Medical University from January 2009 to June 2010 were collected for this study. Expression of MICA/B in these tissue samples was detected by immunohistochemistry; and the relationship between MICA/B expression with clinicopathologic features as well as DFS was analyzed with Kaplan-Meier survival curve. Results: The expression of MICA/B in adjacent paracancerous tissues was negative (0/26), however, it was highly positive in cancer tissues (92/100), and the percentage with high expression was 65%(65/100), the difference was significant (P<0.05). High MICA/B expression rate in stage I was significantly higher than that in stage Ⅱ-Ⅲ (77.55% vs 52.94%，P<0.05), and the high expression rate in stage T1 was also significantly higher than that in stage T2-T4 (75.00% vs 52.27%，P<0.05). High MICA/B expression rate in ER+, PR+ group (with positive number ≥1%) was significantly lower than that in ER- , PR- group (ER：52.38% vs 74.14%，PR：51.35% vs 73.02%，all P<0.05). MICA/B expression was correlated with clinical stages, the expression of ER, PR and tumor size (all P<0.05), but not associated with menopausal status, histological grade and lymph node metastasis (all P>0.05). Over-expression of MICA/B was closely associated with much better 6-year DFS rate in patients no matter with or without targeted therapy (the targeted group: 90.6% vs 72.2%; the untargeted group: 78.4% vs 58.8%, all P<0.05). Conclusion: Over-expression of MICA/B in HER2+ breast cancer tissue is closely related to DFS, which may be served as a potential prognosis indicator for patients with HER2+ breast cancer.
2018, 25(2):182-186.
DOI: 10.3872/j.issn.1007-385X.2018.02.013
Abstract:
慢性粒细胞白血病(chronic myeloid leukemia，CML)是一种髓系造血干细胞恶性克隆性疾病，免疫功能低下是其发生的内在因素，可影响机体免疫系统发挥正常的免疫作用。近年来研究发现，其外周血淋巴细胞亚群分布和功能变化与疾病的发生、发展、转归密切相关。本文就初诊CML患者外周血淋巴细胞亚群分布和功能变化，以及酪氨酸激酶抑制剂（tyrosine kinase inhibitor，TKI）对CML患者外周血淋巴细胞亚群分布、功能及治疗反应的影响等几个方面予以综述。
慢性粒细胞白血病(chronic myeloid leukemia，CML)是一种髓系造血干细胞恶性克隆性疾病，免疫功能低下是其发生的内在因素，可影响机体免疫系统发挥正常的免疫作用。近年来研究发现，其外周血淋巴细胞亚群分布和功能变化与疾病的发生、发展、转归密切相关。本文就初诊CML患者外周血淋巴细胞亚群分布和功能变化，以及酪氨酸激酶抑制剂（tyrosine kinase inhibitor，TKI）对CML患者外周血淋巴细胞亚群分布、功能及治疗反应的影响等几个方面予以综述。
2018, 25(2):187-191.
DOI: 10.3872/j.issn.1007-385X.2018.02.014
Abstract:
CD4+T淋巴细胞是一类重要的免疫细胞，在不同细胞因子的诱导下，可分化为Th1 细胞、Th2 细胞、Th17 细胞和Treg 细胞等。Th17 细胞及Treg 细胞不仅具有多种生物免疫学效应，而且能够分泌不同的细胞因子，各种免疫细胞与细胞因子之间形成复杂网络，介导免疫反应，进行免疫调节，参与免疫相关性疾病的发生发展，如肿瘤、炎症、自身免疫性疾病等。近年来肺癌的发病率呈进行性升高，其中非小细胞肺癌（non-small cell lung cancer，NSCLC）占肺癌的比例最高。因此，本文将对Th17 细胞和Treg 细胞的分化及特点及在NSCLC中的免疫调节作用作一综述。
CD4+T淋巴细胞是一类重要的免疫细胞，在不同细胞因子的诱导下，可分化为Th1 细胞、Th2 细胞、Th17 细胞和Treg 细胞等。Th17 细胞及Treg 细胞不仅具有多种生物免疫学效应，而且能够分泌不同的细胞因子，各种免疫细胞与细胞因子之间形成复杂网络，介导免疫反应，进行免疫调节，参与免疫相关性疾病的发生发展，如肿瘤、炎症、自身免疫性疾病等。近年来肺癌的发病率呈进行性升高，其中非小细胞肺癌（non-small cell lung cancer，NSCLC）占肺癌的比例最高。因此，本文将对Th17 细胞和Treg 细胞的分化及特点及在NSCLC中的免疫调节作用作一综述。
2018, 25(2):192-197.
DOI: 10.3872/j.issn.1007-385X.2018.02.015
Abstract:
女性肿瘤因大多数早期病变隐蔽，且缺乏有效的筛查方法，待确诊时多数患者已发展为中晚期，严重威胁着女性健康及生活质量。单一肿瘤标志物检测的敏感性和特异性都不高，不利于肿瘤的筛查和早期诊断。因此开发多种标志物的联合检测技术对女性肿瘤的早期诊断和早期治疗有重要意义。本文综述了女性肿瘤(乳腺癌、宫颈癌、子宫内膜癌、卵巢癌)肿瘤标志物及其联合检测的最新研究进展，分析了其在肿瘤早期诊断中的临床价值和应用前景。
女性肿瘤因大多数早期病变隐蔽，且缺乏有效的筛查方法，待确诊时多数患者已发展为中晚期，严重威胁着女性健康及生活质量。单一肿瘤标志物检测的敏感性和特异性都不高，不利于肿瘤的筛查和早期诊断。因此开发多种标志物的联合检测技术对女性肿瘤的早期诊断和早期治疗有重要意义。本文综述了女性肿瘤(乳腺癌、宫颈癌、子宫内膜癌、卵巢癌)肿瘤标志物及其联合检测的最新研究进展，分析了其在肿瘤早期诊断中的临床价值和应用前景。
2018, 25(2):198-205.
DOI: 10.3872/j.issn.1007-385X.2018.02.016
Abstract:
溶瘤腺病毒是指经过基因工程改造的腺病毒，其能够选择性地在肿瘤细胞中复制和表达，从而溶解肿瘤细胞;其可经过基因和衣壳蛋白层面的改造，特异性地结合和杀伤肿瘤细胞。自1996 年世界上第一例溶瘤腺病毒ONXY-015 开展临床研究以来，腺病毒在国内外广泛地应用于科学研究及转化应用，已有多个国家批准其在临床肿瘤治疗中使用，使用范围涉及到多种实体瘤。溶瘤腺病毒的改造方式多种多样，本文对溶瘤腺病毒治疗肿瘤的改造方法，如腺病毒的包膜蛋白进行修饰、腺病毒的结构基因进行改造、插入肿瘤特异性启动子、携带治疗基因与携带短发夹RNA和包括溶瘤病毒的多措施联合等研究进展作一综述。
溶瘤腺病毒是指经过基因工程改造的腺病毒，其能够选择性地在肿瘤细胞中复制和表达，从而溶解肿瘤细胞;其可经过基因和衣壳蛋白层面的改造，特异性地结合和杀伤肿瘤细胞。自1996 年世界上第一例溶瘤腺病毒ONXY-015 开展临床研究以来，腺病毒在国内外广泛地应用于科学研究及转化应用，已有多个国家批准其在临床肿瘤治疗中使用，使用范围涉及到多种实体瘤。溶瘤腺病毒的改造方式多种多样，本文对溶瘤腺病毒治疗肿瘤的改造方法，如腺病毒的包膜蛋白进行修饰、腺病毒的结构基因进行改造、插入肿瘤特异性启动子、携带治疗基因与携带短发夹RNA和包括溶瘤病毒的多措施联合等研究进展作一综述。
2018, 25(2):206-208.
DOI: 10.3872/j.issn.1007-385X.2018.02.017
Abstract:
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- 《中国肿瘤生物治疗杂志》
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- 刊号：ISSN 1007-385X
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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.