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Volume 26,Issue 10,2019 Table of Contents
2019, 26(10):1053-1061.
DOI: 10.3872/j.issn.1007-385X.2019.10.001
Abstract:
[Abstract] Nano-antibodies (Nbs) were first discovered in the peripheral blood of alpacas. Compared with traditional antibodies, Nbs have the characteristics of small volume, good stability, strong tissue permeability, and easy production through microbial systems, etc.They are currently the smallest known functional antigen-specific binding fragments. Therefore, Nbs have been considered as valuable proteins in recent years and widely used in many fields, such as basic research, new drug development, disease treatment and so on.This article reviews the structural and biochemical properties of Nbs and the research progress on Nbs in the fields of tumor diagnosis and treatment, as well as their application prospect.
[Abstract] Nano-antibodies (Nbs) were first discovered in the peripheral blood of alpacas. Compared with traditional antibodies, Nbs have the characteristics of small volume, good stability, strong tissue permeability, and easy production through microbial systems, etc.They are currently the smallest known functional antigen-specific binding fragments. Therefore, Nbs have been considered as valuable proteins in recent years and widely used in many fields, such as basic research, new drug development, disease treatment and so on.This article reviews the structural and biochemical properties of Nbs and the research progress on Nbs in the fields of tumor diagnosis and treatment, as well as their application prospect.
2019, 26(10):1062-1067.
DOI: 10.3872/j.issn.1007-385X.2019.10.002
Abstract:
[Abstract] Objective: To investigate the role and molecular mechanism of miR-520d in reversing the chemoresistance of triple negative breast cancer (TNBC) by regulating autophagy. Methods: Docetaxel (Doc) resistant cell lines MDA-MB-231/Doc and MDA-MB-468/Doc were constructed by using human TNBC cell lines MDA-MB-231 and MDA-MB-468 as parental cells, and the cells were divided into blank group (parental cells), control group (drug-resistant group), and miR-520d over-expression group. The expression levels of miR-520d in cells of the blank and drug-resistant groups were detected by qPCR. The Doc-sensitivity of resistant cells over-expressing miR-520d was detected by MTT assay. After MDC staining, the generation of autophagosome in cells was observed under fluorescence microscopy; the number of miR-520d over-expressed resistant cells with positive LC3 expression was observed under confocal microscopy. The luciferase reporter gene assay was used to verify the targeting relationship between miR-520d and Beclin1. The effect of miR-520d mimics on the expression of autophagy-associated protein Beclin1, and LC3Ⅰ, LC3Ⅱ in cells was detected by WB assay.Results: The results of qPCR showed that the expression of miR-520d in the drug-resistant TNBC cells was significantly lower than that of normal cells (P<0.01). In drug-resistant cells over-expressing miR-520d, the Doc-sensitivity was significantly improved,while the autophagy activity was significantly reduced (all P<0.01). At the same time, luciferase experiments demonstrated that Beclin1 was a possible target molecule of miR-520d (P<0.05). WB results showed that the combination of docetaxel and miR-520d mimics reduced the LC3-II/I ratio and the expression of autophagy protein Beclin1 in drug-resistant TNBC cells (all P<0.05). Conclusion: The regulation of miR-520d levels may alter the expression of autophagy protein Beclin1, thereby reversing Doc chemotherapy resistance in TNBC cells.
[Abstract] Objective: To investigate the role and molecular mechanism of miR-520d in reversing the chemoresistance of triple negative breast cancer (TNBC) by regulating autophagy. Methods: Docetaxel (Doc) resistant cell lines MDA-MB-231/Doc and MDA-MB-468/Doc were constructed by using human TNBC cell lines MDA-MB-231 and MDA-MB-468 as parental cells, and the cells were divided into blank group (parental cells), control group (drug-resistant group), and miR-520d over-expression group. The expression levels of miR-520d in cells of the blank and drug-resistant groups were detected by qPCR. The Doc-sensitivity of resistant cells over-expressing miR-520d was detected by MTT assay. After MDC staining, the generation of autophagosome in cells was observed under fluorescence microscopy; the number of miR-520d over-expressed resistant cells with positive LC3 expression was observed under confocal microscopy. The luciferase reporter gene assay was used to verify the targeting relationship between miR-520d and Beclin1. The effect of miR-520d mimics on the expression of autophagy-associated protein Beclin1, and LC3Ⅰ, LC3Ⅱ in cells was detected by WB assay.Results: The results of qPCR showed that the expression of miR-520d in the drug-resistant TNBC cells was significantly lower than that of normal cells (P<0.01). In drug-resistant cells over-expressing miR-520d, the Doc-sensitivity was significantly improved,while the autophagy activity was significantly reduced (all P<0.01). At the same time, luciferase experiments demonstrated that Beclin1 was a possible target molecule of miR-520d (P<0.05). WB results showed that the combination of docetaxel and miR-520d mimics reduced the LC3-II/I ratio and the expression of autophagy protein Beclin1 in drug-resistant TNBC cells (all P<0.05). Conclusion: The regulation of miR-520d levels may alter the expression of autophagy protein Beclin1, thereby reversing Doc chemotherapy resistance in TNBC cells.
2019, 26(10):1068-1074.
DOI: 10.3872/j.issn.1007-385X.2019.10.003
Abstract:
[Abstract] Objective: To investigate whether long non-coding RNA (lncRNA) FOXD2-AS1 targets miR-506-5p to regulate proliferation and apoptosis of cervical cancer cells. Methods: Human normal cervical cells Ect1/E6E7 and cervical cancer cell lines (HeLa, Siha and Caski) were cultured in vitro, and the expression levels of FOXD2-AS1 and miR-506-5p in cells were detected by qPCR. The cervical cancer cells with FOXD2-AS1 knockdown and miR-506-5p over-expression were constructed by liposome transfection technology, and the proliferation and apoptosis of cells were detected by MTT assay and flow cytometry respectively, the expression of proliferation-related proteins CyclinD1, p21, p27 and apoptosis-related proteins Bcl-2, BAX, cleaved-capase-3 were detected by WB. Dual luciferase reporter assay was used to verify whether FOXD2-AS1 would target miR-506-5p; and the effects of simultaneous inhibition of FOXD2-AS1 and miR-506-5p on proliferation and apoptosis of cervical cancer cells were also analyzed. Results: Compared with Ect1/E6E7 cells, the expression of FOXD2-AS1 significantly increased while the expression of miR-506-5p significantly decreased in cervical cancer HeLa, Siha and Caski cells (all P<0.01). FOXD2-AS1 knockdown significantly inhibited the protein expressions of CyclinD1, Bcl-2 and cell proliferationin cervical cancer cells, but promoted the protein expressions of p21, p27, BAX, cleavedcapase-3, and cell apoptosis (all P<0.01). miR-506-5p over-expression significantly inhibited the protein expressions of CyclinD1, Bcl-2 and cell proliferation in cervical cancer cells, but promoted the protein expressions of p21, BAX, and cell apoptosis (all P<0.01).Dual luciferase reporter gene assay confirmed that FOXD2-AS1 negatively regulated the expression of miR-506-5p in cervical cancer cells (P<0.01). Inhibition of miR-506-5p expression reversed the effect of FOXD2-AS1 knockdown on proliferation and apoptosis of cervical cancer cell (P<0.01). Conclusion: FOXD2-AS1 modulates proliferation and apoptosis of cervical cancer cells by negatively regulating the expression of miR-506-5p.
[Abstract] Objective: To investigate whether long non-coding RNA (lncRNA) FOXD2-AS1 targets miR-506-5p to regulate proliferation and apoptosis of cervical cancer cells. Methods: Human normal cervical cells Ect1/E6E7 and cervical cancer cell lines (HeLa, Siha and Caski) were cultured in vitro, and the expression levels of FOXD2-AS1 and miR-506-5p in cells were detected by qPCR. The cervical cancer cells with FOXD2-AS1 knockdown and miR-506-5p over-expression were constructed by liposome transfection technology, and the proliferation and apoptosis of cells were detected by MTT assay and flow cytometry respectively, the expression of proliferation-related proteins CyclinD1, p21, p27 and apoptosis-related proteins Bcl-2, BAX, cleaved-capase-3 were detected by WB. Dual luciferase reporter assay was used to verify whether FOXD2-AS1 would target miR-506-5p; and the effects of simultaneous inhibition of FOXD2-AS1 and miR-506-5p on proliferation and apoptosis of cervical cancer cells were also analyzed. Results: Compared with Ect1/E6E7 cells, the expression of FOXD2-AS1 significantly increased while the expression of miR-506-5p significantly decreased in cervical cancer HeLa, Siha and Caski cells (all P<0.01). FOXD2-AS1 knockdown significantly inhibited the protein expressions of CyclinD1, Bcl-2 and cell proliferationin cervical cancer cells, but promoted the protein expressions of p21, p27, BAX, cleavedcapase-3, and cell apoptosis (all P<0.01). miR-506-5p over-expression significantly inhibited the protein expressions of CyclinD1, Bcl-2 and cell proliferation in cervical cancer cells, but promoted the protein expressions of p21, BAX, and cell apoptosis (all P<0.01).Dual luciferase reporter gene assay confirmed that FOXD2-AS1 negatively regulated the expression of miR-506-5p in cervical cancer cells (P<0.01). Inhibition of miR-506-5p expression reversed the effect of FOXD2-AS1 knockdown on proliferation and apoptosis of cervical cancer cell (P<0.01). Conclusion: FOXD2-AS1 modulates proliferation and apoptosis of cervical cancer cells by negatively regulating the expression of miR-506-5p.
2019, 26(10):1075-1082.
DOI: 10.3872/j.issn.1007-385X.2019.10.004
Abstract:
[Abstract] Objective: To investigate the effects and mechanisms of miR-129-5p on invasion, migration and epithelial-mesenchymal transition (EMT) of cervical cancer HeLa cells. Methods:Cervical cancer HeLa cells were selected. The target gene of miR-129-5p was screened by bioinformatics prediction software, and the targeting relationship between miR-129-5p and MAPK1 was verified by dual luciferase reporter gene assay. HeLa cells were transfected with miR-129-5p mimic, miR-129-5p inhibitor and pcDNA-MAPK1 alone or in combination.The expressions of miR-129-5p and MAPK1 in HeLa cells were detected by qPCR; the invasion and migration ability of HeLa cells were detected by Transwell and scratch-healing experiments, respectively; and the expressions of E-cadherin, N-cadherin,MAPK1, STAT3 and Bcl-xL were detected by WB. The subcutaneous xenograft model of HeLa cells in nude mice was constructed to observe the effect of miR-129-5p over-expression on the growth of transplanted tumors. The expressions of EMT and MAPK1 pathwayrelated proteins in transplanted tumor tissues were detected by WB. Results: miR-129-5p could bind with the 3'UTR region of MAPK1,and over-expression of miR-129-5p targetedly inhibited the expression of MAPK1 (P<0.01). Compared with the control group, the number of invasive cells in the miR-129-5p mimic group decreased (P<0.01), the scratch healing rate decreased (all P<0.01); The expression of E-cadherin was up-regulated, and the expressions of N-cadherin, MAPK1, STAT3 and Bcl-xL were down-regulated (all P<0.01), while co-transfection of MAPK1 reversed the above phenomenon.The nude mice HeLa cell xenograft model was successfully established.Compared with the control group, the tumor mass of the miR-128-3p mimic group was reduced; the expression of E-cadherin was up-regulated in tumor tissues, while the expressions of N-cadherin, MAPK1, STAT3 and Bcl-xL were down-regulated (all P<0.01).Conclusion: Over-expression of miR-129-5p inhibits invasion, migration and epithelial-mesenchymal transition of cervical cancer HeLa cells by targeting MAPK1.
[Abstract] Objective: To investigate the effects and mechanisms of miR-129-5p on invasion, migration and epithelial-mesenchymal transition (EMT) of cervical cancer HeLa cells. Methods:Cervical cancer HeLa cells were selected. The target gene of miR-129-5p was screened by bioinformatics prediction software, and the targeting relationship between miR-129-5p and MAPK1 was verified by dual luciferase reporter gene assay. HeLa cells were transfected with miR-129-5p mimic, miR-129-5p inhibitor and pcDNA-MAPK1 alone or in combination.The expressions of miR-129-5p and MAPK1 in HeLa cells were detected by qPCR; the invasion and migration ability of HeLa cells were detected by Transwell and scratch-healing experiments, respectively; and the expressions of E-cadherin, N-cadherin,MAPK1, STAT3 and Bcl-xL were detected by WB. The subcutaneous xenograft model of HeLa cells in nude mice was constructed to observe the effect of miR-129-5p over-expression on the growth of transplanted tumors. The expressions of EMT and MAPK1 pathwayrelated proteins in transplanted tumor tissues were detected by WB. Results: miR-129-5p could bind with the 3'UTR region of MAPK1,and over-expression of miR-129-5p targetedly inhibited the expression of MAPK1 (P<0.01). Compared with the control group, the number of invasive cells in the miR-129-5p mimic group decreased (P<0.01), the scratch healing rate decreased (all P<0.01); The expression of E-cadherin was up-regulated, and the expressions of N-cadherin, MAPK1, STAT3 and Bcl-xL were down-regulated (all P<0.01), while co-transfection of MAPK1 reversed the above phenomenon.The nude mice HeLa cell xenograft model was successfully established.Compared with the control group, the tumor mass of the miR-128-3p mimic group was reduced; the expression of E-cadherin was up-regulated in tumor tissues, while the expressions of N-cadherin, MAPK1, STAT3 and Bcl-xL were down-regulated (all P<0.01).Conclusion: Over-expression of miR-129-5p inhibits invasion, migration and epithelial-mesenchymal transition of cervical cancer HeLa cells by targeting MAPK1.
2019, 26(10):1083-1088.
DOI: 10.3872/j.issn.1007-385X.2019.10.005
Abstract:
[Abstract] Objective: To construct indocyanine green-loaded silica nanoparticles (ICG@MSNs) and evaluate their killing effect on cervical cancer HeLa cells. Methods: Mesoporous silica nanoparticles (MSNs) were synthesized by template method, and indocyanine green (ICG) containing photothermal agent was loaded to prepare ICG@MSNs with photothermal effect, which were applied in the research of HeLa cells in vitro. Results: The particle of ICG@MSNs was uniform and in regular spherical shape with the size about 200 nm. ICG@MSNs was similar photothermal effect with pure ICG. Cell endocytosis experiments showed that ICG encapsulated in silica nanoparticles is more likely to be endocytosed by tumor cells, and then played a photothermal role in killing cervical cancer HeLa cells. On the other hand, cytotoxicity experiments showed that under the irradiation of 808 nm laser, ICG@MSNs significantly increased cytotoxicity, which could significantly kill cervical cancer HeLa cells. Conclusion: ICG@MSNs has good stability and biocompatibility,as well as good thermogenesis. It’s photothermal treatment effect on tumor is obvious, which has a good prospect for the treatment of cervical cancer.
[Abstract] Objective: To construct indocyanine green-loaded silica nanoparticles (ICG@MSNs) and evaluate their killing effect on cervical cancer HeLa cells. Methods: Mesoporous silica nanoparticles (MSNs) were synthesized by template method, and indocyanine green (ICG) containing photothermal agent was loaded to prepare ICG@MSNs with photothermal effect, which were applied in the research of HeLa cells in vitro. Results: The particle of ICG@MSNs was uniform and in regular spherical shape with the size about 200 nm. ICG@MSNs was similar photothermal effect with pure ICG. Cell endocytosis experiments showed that ICG encapsulated in silica nanoparticles is more likely to be endocytosed by tumor cells, and then played a photothermal role in killing cervical cancer HeLa cells. On the other hand, cytotoxicity experiments showed that under the irradiation of 808 nm laser, ICG@MSNs significantly increased cytotoxicity, which could significantly kill cervical cancer HeLa cells. Conclusion: ICG@MSNs has good stability and biocompatibility,as well as good thermogenesis. It’s photothermal treatment effect on tumor is obvious, which has a good prospect for the treatment of cervical cancer.
HAN Zheng
,
HUANG Xiaodong
,
LIU Meng
,
ZHU Qingxi
,
TAN Jie
,
LIUWeijie
,
CHENWei
,
ZOUYanli
,
CAI Yishan
,
HUANG Shasha
,
TIAN Xia
2019, 26(10):1089-1094.
DOI: 10.3872/j.issn.1007-385X.2019.10.006
Abstract:
[Abstract] Objective: To explore the effects of noscapine (Nos) on the expression of cadherin 17 (CDH17) in colon cancer SW480 cells and the mechanism of Nos on cell migration. Methods: SW480 cells were divided into the control group, empty vector (si-EV)group, CDH17 interference (si-CDH17) group, Nos treatment group, and CDH17 interference+Nos treatment (si-CDH17+Nos) group.Small interfering RNA (siRNA) was used to knockdown CDH17, and the selected concentration of Nos was (55.30±2.21) μg/ml (IC50).The mRNA expression of CDH17 was detected by qPCR; the apoptosis and migration abilities of SW480 cells were observed by Hoechst33258 staining and Transwell assay; the contents of VEGF, MMP2 and MMP9 in SW480 cells were measured by ELISA, and the protein expressions of CDH17, Wnt3a and β-catenin were determined by WB. Results: Compared with the control group, mRNA and protein expressions of CDH17 obviously decreased, cell apoptosis and migration significantly reduced, while the contents of VEGF, MMP2 and MMP9 as well as the protein expressions of Wnt3a and β-catenin significantly decreased in Nos treatment group, si-CDH17 group and si-CDH17+Nos treatment group (all P<0.01).The effect of si-CDH17+Nos treatment was more significant than that of si-CDH17 (P<0.01). Conclusion: Nos induces apoptosis and inhibits the migration of human colon cancer SW480 cells, which may be related to the down-regulation of CDH17 expression and inhibition of the Wnt3a/β-catenin signaling pathway.
[Abstract] Objective: To explore the effects of noscapine (Nos) on the expression of cadherin 17 (CDH17) in colon cancer SW480 cells and the mechanism of Nos on cell migration. Methods: SW480 cells were divided into the control group, empty vector (si-EV)group, CDH17 interference (si-CDH17) group, Nos treatment group, and CDH17 interference+Nos treatment (si-CDH17+Nos) group.Small interfering RNA (siRNA) was used to knockdown CDH17, and the selected concentration of Nos was (55.30±2.21) μg/ml (IC50).The mRNA expression of CDH17 was detected by qPCR; the apoptosis and migration abilities of SW480 cells were observed by Hoechst33258 staining and Transwell assay; the contents of VEGF, MMP2 and MMP9 in SW480 cells were measured by ELISA, and the protein expressions of CDH17, Wnt3a and β-catenin were determined by WB. Results: Compared with the control group, mRNA and protein expressions of CDH17 obviously decreased, cell apoptosis and migration significantly reduced, while the contents of VEGF, MMP2 and MMP9 as well as the protein expressions of Wnt3a and β-catenin significantly decreased in Nos treatment group, si-CDH17 group and si-CDH17+Nos treatment group (all P<0.01).The effect of si-CDH17+Nos treatment was more significant than that of si-CDH17 (P<0.01). Conclusion: Nos induces apoptosis and inhibits the migration of human colon cancer SW480 cells, which may be related to the down-regulation of CDH17 expression and inhibition of the Wnt3a/β-catenin signaling pathway.
2019, 26(10):1095-1100.
DOI: 10.3872/j.issn.1007-385X.2019.10.007
Abstract:
[Abstract] Objective: To study the inhibitory effect of gigantol on proliferation, migration and invasion of human osteosarcoma U20S cells and to explore the mechanism. Methods: After being treated with different concentrations (10, 25, 50, 75, 100, 150 μmol/L) of gigantol for 24 and 48 h, the proliferation of U20S cells was detected by CCK-8 assay. Transwell assay was used to detect the effects of 25 μmol/L and 50 μmol/L gigantol on the migration and invasion abilities of U20S cells. The lipopolysaccharide (LPS) was used to induce inflammatory reaction in U20S cells before gigantol treatment; qPCR and WB were used to detect the mRNA and protein expressions of NF-κB (p65), TNF-α, IL-6 and PRL-3, respectively. Results: Different concentrations of gigantol could all inhibit the proliferation of sarcoma U20S cells at different time (P<0.05 or P<0.01). The 25 μmol/L and 50 μmol/L of gigantol could significantly inhibit the migration and invasion of osteosarcoma U20S cells (all P<0.01); at the same time, it could inhibit the protein expressions of NF- κB, TNF- α , IL-6 and PRL-3 (P<0.05 or P<0.01). After LPS induction, the mRNA and protein expressions of NF- κB, TNF- α , IL-6 and PRL-3 in U20S cells were significantly increased (all P<0.01); however, the consequent treatment with gigantol (25 and 50 μmol/L) reversed the effects of LPS on U20S cells obviously (P<0.05 or P<0.01). Conclusion:Gigantol can inhibit the proliferation, migration and invasion of osteosarcoma U20S cells, and its mechanism may be related to the regulation of NF-κB/PRL-3 signaling pathway.
[Abstract] Objective: To study the inhibitory effect of gigantol on proliferation, migration and invasion of human osteosarcoma U20S cells and to explore the mechanism. Methods: After being treated with different concentrations (10, 25, 50, 75, 100, 150 μmol/L) of gigantol for 24 and 48 h, the proliferation of U20S cells was detected by CCK-8 assay. Transwell assay was used to detect the effects of 25 μmol/L and 50 μmol/L gigantol on the migration and invasion abilities of U20S cells. The lipopolysaccharide (LPS) was used to induce inflammatory reaction in U20S cells before gigantol treatment; qPCR and WB were used to detect the mRNA and protein expressions of NF-κB (p65), TNF-α, IL-6 and PRL-3, respectively. Results: Different concentrations of gigantol could all inhibit the proliferation of sarcoma U20S cells at different time (P<0.05 or P<0.01). The 25 μmol/L and 50 μmol/L of gigantol could significantly inhibit the migration and invasion of osteosarcoma U20S cells (all P<0.01); at the same time, it could inhibit the protein expressions of NF- κB, TNF- α , IL-6 and PRL-3 (P<0.05 or P<0.01). After LPS induction, the mRNA and protein expressions of NF- κB, TNF- α , IL-6 and PRL-3 in U20S cells were significantly increased (all P<0.01); however, the consequent treatment with gigantol (25 and 50 μmol/L) reversed the effects of LPS on U20S cells obviously (P<0.05 or P<0.01). Conclusion:Gigantol can inhibit the proliferation, migration and invasion of osteosarcoma U20S cells, and its mechanism may be related to the regulation of NF-κB/PRL-3 signaling pathway.
2019, 26(10):1101-1106.
DOI: 10.3872/j.issn.1007-385X.2019.10.008
Abstract:
[Abstract] Objective: To investigate the effect of miR-144-3p modulating proliferation, migration and apoptosis of liver cancer Huh-7 cells through blocking frizzled class receptor 4 (FZD4)/Wnt/β -catenin pathway and the possible mechanism. Methods: A total of 18 pairs of cancer tissues and corresponding para-cancerous tissues from liver cancer patients, who underwent surgery in Workers' Hospital of Liuzhou City from March 2012 to July 2017, were collected for this study; in addition, hepatic cancer cell lines (Huh-7, SMMC7721 and MHCC97) and human normal liver epithelial cell line THLE-3 were also collected. The expression of miR-144-3p in liver cancer tissues and cell lines was detected by qPCR. MiR-144-3p mimics/inhibitor and FZD4 siRNA were transfected into liver cancer Huh-7 cells; the proliferation, migration and apoptosis of Huh-7 cells were evaluated by CCK-8 assay, Transwell assay, wound healing assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. The interaction between miR-144-3p and FZD4 was verified by dual-luciferase reporter gene assay. Results: The expression of miR-144-3p was down-regulated in liver cancer tissues and cell lines (P<0.05 or P<0.01). Over-expression of miR-144-3p significantly inhibited cell proliferation viability, migration but induced apoptosis of Huh-7 cells (all P<0.01). Moreover, dual-luciferase reporter gene assay showed that miR-144-3p directly interacted with FZD4 and suppressed its expression. Furthermore, in vitro experiments verified that miR-144-3p targeted FZD4 to suppress the proliferation,migration and promote apoptosis of Huh-7 cells via blocking Wnt/β -catenin pathway (all P<0.01). Conclusion: miR-144-3p inhibits malignant biological behaviors of liver cancer Huh-7 cells via blocking Wnt/FZD4/β-catenin signaling pathway, which may provide potential molecular targets for early diagnosis or treatment of liver cancer.
[Abstract] Objective: To investigate the effect of miR-144-3p modulating proliferation, migration and apoptosis of liver cancer Huh-7 cells through blocking frizzled class receptor 4 (FZD4)/Wnt/β -catenin pathway and the possible mechanism. Methods: A total of 18 pairs of cancer tissues and corresponding para-cancerous tissues from liver cancer patients, who underwent surgery in Workers' Hospital of Liuzhou City from March 2012 to July 2017, were collected for this study; in addition, hepatic cancer cell lines (Huh-7, SMMC7721 and MHCC97) and human normal liver epithelial cell line THLE-3 were also collected. The expression of miR-144-3p in liver cancer tissues and cell lines was detected by qPCR. MiR-144-3p mimics/inhibitor and FZD4 siRNA were transfected into liver cancer Huh-7 cells; the proliferation, migration and apoptosis of Huh-7 cells were evaluated by CCK-8 assay, Transwell assay, wound healing assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. The interaction between miR-144-3p and FZD4 was verified by dual-luciferase reporter gene assay. Results: The expression of miR-144-3p was down-regulated in liver cancer tissues and cell lines (P<0.05 or P<0.01). Over-expression of miR-144-3p significantly inhibited cell proliferation viability, migration but induced apoptosis of Huh-7 cells (all P<0.01). Moreover, dual-luciferase reporter gene assay showed that miR-144-3p directly interacted with FZD4 and suppressed its expression. Furthermore, in vitro experiments verified that miR-144-3p targeted FZD4 to suppress the proliferation,migration and promote apoptosis of Huh-7 cells via blocking Wnt/β -catenin pathway (all P<0.01). Conclusion: miR-144-3p inhibits malignant biological behaviors of liver cancer Huh-7 cells via blocking Wnt/FZD4/β-catenin signaling pathway, which may provide potential molecular targets for early diagnosis or treatment of liver cancer.
2019, 26(10):1107-1112.
DOI: 10.3872/j.issn.1007-385X.2019.10.009
Abstract:
[Abstract] Objective: To investigate the influence of miR-520a-3p on paclitaxel (TAX) sensitivity of non-small cell lung cancer (NSCLC) A549/TAX cells via regulating frizzled class receptor 8 (FZD8). Methods: NSCLC A549 cells, TAX-resistant cell line A549/TAX and human lung epithelial HLF-α cells were selected. The expression level of miR-520a-3p in A549 and A549/TAX cells was detected by qPCR. According to different transfection plasmids, the experimental cells were divided into control group, miR-520a-3p mimics group, si-FZ8 group and si-FZD8+miR-520a-3p inhibitor group. After being treated with 6 μmol/L paclitaxel, the proliferation of A549/TAX cells was determined by CCK-8 assay. Flow cytometry with Annexin V-FLTC/PI staining was used to detect the apoptosis level of A549/TAX cells. The expression of FZD8 in A549/TAX cells was detected by WB. The targeting relationship between miR-520a-3p and FZD8 was verified by the dual-luciferase reporter gene system. Results: miR-520a-3p was poorly expressed in TAX-resistant A549/TAX cells (P<0.01), and TAX up-regulated the expression of miR-520a-3p in A549/TAX cells (P<0.01). After the treatment with 6 μmol/L TAX, over-expression of miR-520a-3p significantly inhibited the proliferation of A549/TAX cells and promoted apoptosis (all P<0.01). Dual luciferase reporter gene assay showed that miR-520a-3p targetedly down-regulated the expression of FZD8 (P<0.01). si-FZD8 could significantly inhibit the proliferation and promote cell apoptosis of A549 / TAX cells, thereby enhancing the TAX sensitivity of cells. At the same time, simultaneous knockdown of miR-520a-3p and FZD8 could reverse the enhancement of FZD8 knockdown on TAX sensitivity of A549/TAX cells (P<0.01). Conclusion: miR-520a-3p enhances the TAX sensitivity of A549/TAX cells by down-regulating the expression of FZD8.
[Abstract] Objective: To investigate the influence of miR-520a-3p on paclitaxel (TAX) sensitivity of non-small cell lung cancer (NSCLC) A549/TAX cells via regulating frizzled class receptor 8 (FZD8). Methods: NSCLC A549 cells, TAX-resistant cell line A549/TAX and human lung epithelial HLF-α cells were selected. The expression level of miR-520a-3p in A549 and A549/TAX cells was detected by qPCR. According to different transfection plasmids, the experimental cells were divided into control group, miR-520a-3p mimics group, si-FZ8 group and si-FZD8+miR-520a-3p inhibitor group. After being treated with 6 μmol/L paclitaxel, the proliferation of A549/TAX cells was determined by CCK-8 assay. Flow cytometry with Annexin V-FLTC/PI staining was used to detect the apoptosis level of A549/TAX cells. The expression of FZD8 in A549/TAX cells was detected by WB. The targeting relationship between miR-520a-3p and FZD8 was verified by the dual-luciferase reporter gene system. Results: miR-520a-3p was poorly expressed in TAX-resistant A549/TAX cells (P<0.01), and TAX up-regulated the expression of miR-520a-3p in A549/TAX cells (P<0.01). After the treatment with 6 μmol/L TAX, over-expression of miR-520a-3p significantly inhibited the proliferation of A549/TAX cells and promoted apoptosis (all P<0.01). Dual luciferase reporter gene assay showed that miR-520a-3p targetedly down-regulated the expression of FZD8 (P<0.01). si-FZD8 could significantly inhibit the proliferation and promote cell apoptosis of A549 / TAX cells, thereby enhancing the TAX sensitivity of cells. At the same time, simultaneous knockdown of miR-520a-3p and FZD8 could reverse the enhancement of FZD8 knockdown on TAX sensitivity of A549/TAX cells (P<0.01). Conclusion: miR-520a-3p enhances the TAX sensitivity of A549/TAX cells by down-regulating the expression of FZD8.
2019, 26(10):1113-1119.
DOI: 10.3872/j.issn.1007-385X.2019.10.010
Abstract:
[Abstract] Objective: To investigate the effect of miR-23b/PTEN molecular axis on radio-sensitivity of lung cancer A549 cells and its mechanism. Methods: Lung cancer cell lines NCI-H1650, NCI-H175, Calu-1, LT-P-A-2, MSTO-211H, A549 and human normal lung epithelial cell line BEAS-2B were selected. The expression level of miR-23b in lung cancer cell lines was detected by qPCR. Dual-luciferase reporter gene assay was used to verify the relationship between miR-23b and PTEN. Plasmids miR-23b mimics, miR-23b inhibitor and pcDNA3.1-PTEN were transfected into A549 cells by lipofection; PTEN expression levels in cells was detected by WB. CCK-8,Transwell and Annexin V-FITC/PI staining flow cytometry were used to detect the effect of miR-23b/PTEN axis on proliferation, invasion and apoptosis of A549 cells treated with 60Co γ-ray. Results: miR-23b was upregulated in lung cancer cell lines with the highest expression in A549 cells (P<0.05 or P<0.01). Knockdown of miR-23b reversed the inhibitory effect of 3 Gy 60Co γ-rays on proliferation and invasion of A549 cells, and induced apoptosis (P<0.05 or P<0.01). Dual-luciferase reporter gene assay results confirmed that miR-23b could negatively regulate PTEN (P<0.05). Furthermore, knockdown of miR-23b up-regulated PTEN expression level, and furhter enhanced the inhibitory effect of 3 Gy 60Co γ-ray on the proliferation and invasion of A549 cells as well as induced apoptosis of A549 cells (P<0.05 or P<0.01). Conclusion: Knockdown of miR-23b can enhance the radio-sensitivity of A549 cells, the mechanism of which is that 60Co γ-ray down-regulates the inhibitory effect of miR-23b on PTEN, thereby inhibiting the proliferation, invasion and inducing apoptosis of A549 cells.
[Abstract] Objective: To investigate the effect of miR-23b/PTEN molecular axis on radio-sensitivity of lung cancer A549 cells and its mechanism. Methods: Lung cancer cell lines NCI-H1650, NCI-H175, Calu-1, LT-P-A-2, MSTO-211H, A549 and human normal lung epithelial cell line BEAS-2B were selected. The expression level of miR-23b in lung cancer cell lines was detected by qPCR. Dual-luciferase reporter gene assay was used to verify the relationship between miR-23b and PTEN. Plasmids miR-23b mimics, miR-23b inhibitor and pcDNA3.1-PTEN were transfected into A549 cells by lipofection; PTEN expression levels in cells was detected by WB. CCK-8,Transwell and Annexin V-FITC/PI staining flow cytometry were used to detect the effect of miR-23b/PTEN axis on proliferation, invasion and apoptosis of A549 cells treated with 60Co γ-ray. Results: miR-23b was upregulated in lung cancer cell lines with the highest expression in A549 cells (P<0.05 or P<0.01). Knockdown of miR-23b reversed the inhibitory effect of 3 Gy 60Co γ-rays on proliferation and invasion of A549 cells, and induced apoptosis (P<0.05 or P<0.01). Dual-luciferase reporter gene assay results confirmed that miR-23b could negatively regulate PTEN (P<0.05). Furthermore, knockdown of miR-23b up-regulated PTEN expression level, and furhter enhanced the inhibitory effect of 3 Gy 60Co γ-ray on the proliferation and invasion of A549 cells as well as induced apoptosis of A549 cells (P<0.05 or P<0.01). Conclusion: Knockdown of miR-23b can enhance the radio-sensitivity of A549 cells, the mechanism of which is that 60Co γ-ray down-regulates the inhibitory effect of miR-23b on PTEN, thereby inhibiting the proliferation, invasion and inducing apoptosis of A549 cells.
2019, 26(10):1120-1127.
DOI: 10.3872/j.issn.1007-385X.2019.10.011
Abstract:
[Abstract] Objective: To investigate the expression of microRNA (miR) -760 in human cervical squamous cell carcinoma (CSCC) tissues and cells, and it’s effects on the proliferation, apoptosis, invasion, migration and epithelial-mesenchymal transition (EMT) of SiHa cells, as well as its molecular mechanism. Methods: Eighty pairs of CSCC cancerous and corresponding para-cancerous tissue specimens which were pathologically confirmed and 40 cases of normal cervical tissue specimens obtained by myomectomy in Liaocheng Maternal and Child Health Hospital of Shandong Province from April 2015 to August 2018 were selected. The expression of miR-760 in CSCC tissues, para-cancerous tissues and normal cervical tissues, human CSCC cell lines (SiHa, HCC94) and human cervical squamous epithelial immortalized H8 cells were detected by qPCR, and the relationship between miR-760 and clinicopathological characteristics of CSCC patients was analyzed. miR-760 mimics and NC-mimics plasmids were transfected into SiHa cells by liposome transfection.The expression of miR-760 in SiHa cells was detected by qPCR, the proliferation activity and apoptosis rate were detected by CCK-8 test and flow cytometry, respectively. The invasion and migration of SiHa cells were detected by Transwell assay. The expres-sions of EMT-related proteins, such as E-cadherin, vimentin and N-cadherin, in SiHa cells were detected by WB. Bioinformatics was used to predict the targeting relationship between FOXA1 and miR-760, and double luciferase reporter gene assay was used to verify the direct regulation of miR-760 on FOXA1. Results: The expression of miR-760 in CSCC tissues was significantly lower than that in para-cancerous tissues and normal cervical tissues (all P<0.01), and the expression of miR-760 was closely related to lymphnode metastasis and clinical stage (all P<0.01). The expression of miR-760 in SiHa and HCC94 cells was significantly lower than that in H8 cells (all P<0.01). Up-regulation of the expression of miR-760 could significantly inhibit the proliferation, invasion and migration of SiHa cells (all P<0.01), promote apoptosis (P<0.01), up-regulate the expression of E-cadherin protein (P<0.01), and down-regulate the protein expressions of vimentin and N-cadherin (all P<0.01).FOXA1 was a direct target gene of miR-760 (P<0.01). Up-regulation of miR-760 significantly inhibited the mRNA and protein expressions of FOXA1 in SiHa cells (all P<0.05). Conclusion: The expression of miR-760 is down-regulated in CSCC tissues and cells, and it can regulate the proliferation, invasion, migration and apoptosis of CSCC cells by targeting FOXA1.
[Abstract] Objective: To investigate the expression of microRNA (miR) -760 in human cervical squamous cell carcinoma (CSCC) tissues and cells, and it’s effects on the proliferation, apoptosis, invasion, migration and epithelial-mesenchymal transition (EMT) of SiHa cells, as well as its molecular mechanism. Methods: Eighty pairs of CSCC cancerous and corresponding para-cancerous tissue specimens which were pathologically confirmed and 40 cases of normal cervical tissue specimens obtained by myomectomy in Liaocheng Maternal and Child Health Hospital of Shandong Province from April 2015 to August 2018 were selected. The expression of miR-760 in CSCC tissues, para-cancerous tissues and normal cervical tissues, human CSCC cell lines (SiHa, HCC94) and human cervical squamous epithelial immortalized H8 cells were detected by qPCR, and the relationship between miR-760 and clinicopathological characteristics of CSCC patients was analyzed. miR-760 mimics and NC-mimics plasmids were transfected into SiHa cells by liposome transfection.The expression of miR-760 in SiHa cells was detected by qPCR, the proliferation activity and apoptosis rate were detected by CCK-8 test and flow cytometry, respectively. The invasion and migration of SiHa cells were detected by Transwell assay. The expres-sions of EMT-related proteins, such as E-cadherin, vimentin and N-cadherin, in SiHa cells were detected by WB. Bioinformatics was used to predict the targeting relationship between FOXA1 and miR-760, and double luciferase reporter gene assay was used to verify the direct regulation of miR-760 on FOXA1. Results: The expression of miR-760 in CSCC tissues was significantly lower than that in para-cancerous tissues and normal cervical tissues (all P<0.01), and the expression of miR-760 was closely related to lymphnode metastasis and clinical stage (all P<0.01). The expression of miR-760 in SiHa and HCC94 cells was significantly lower than that in H8 cells (all P<0.01). Up-regulation of the expression of miR-760 could significantly inhibit the proliferation, invasion and migration of SiHa cells (all P<0.01), promote apoptosis (P<0.01), up-regulate the expression of E-cadherin protein (P<0.01), and down-regulate the protein expressions of vimentin and N-cadherin (all P<0.01).FOXA1 was a direct target gene of miR-760 (P<0.01). Up-regulation of miR-760 significantly inhibited the mRNA and protein expressions of FOXA1 in SiHa cells (all P<0.05). Conclusion: The expression of miR-760 is down-regulated in CSCC tissues and cells, and it can regulate the proliferation, invasion, migration and apoptosis of CSCC cells by targeting FOXA1.
2019, 26(10):1128-1133.
DOI: 10.3872/j.issn.1007-385X.2019.10.012
Abstract:
[Abstract] Objective: To screen differentially expressed lncRNA, miRNA and mRNA in colorectal cancer (CRC) in TCGA database,and to explore their relationship with CRC prognosis and related biological functions. Methods: RNA sequencing (RNA-Seq) data and miRNA-Seq data of CRC samples were downloaded from the TCGA database and analyzed, and differentially expressed lncRNA, miRNA and mRNA were screened by R program. The lncRNA-miRNA-mRNA ceRNA network in CRC was constructed by analyzing and integrating the relationships between differentially expressed RNAs through miRcode, TargetScan and miRTarbase databases.Kaplan-Meier method was used to analyze the relationship between the expression of lncRNA, miRNA, mRNA in ceRNA network and the survival prognosis of patients.Finally, the signal pathways involved in the occurrence and development of CRC were analyzed by GSEA functional enrichment analysis software. Results: A total of 614 differentially expressed lncRNAs, 244 differentially expressed miRNAs,and 12 672 differentially expressed mRNAs in CRC were identified; a ceRNA network consisting of 139 lncRNAs, 37 miRNAs and 228 mRNAs was constructed;It was found that 58 lncRNAs, 23 miRNAs, and 150 mRNAs were associated with the prognosis of CRC.The results of GSEA enrichment analysis showed that mRNA was mainly involved in signaling pathways such as Notch, Hedgehog and TGF-β. Conclusion: CRC-related ceRNA network was successfully constructed and lncRNAs, miRNAs and mRNAs associated with CRC prognosis were screened. It provides a valuable preliminary basis for further in-depth clinical research and basic experimental research on CRC.
[Abstract] Objective: To screen differentially expressed lncRNA, miRNA and mRNA in colorectal cancer (CRC) in TCGA database,and to explore their relationship with CRC prognosis and related biological functions. Methods: RNA sequencing (RNA-Seq) data and miRNA-Seq data of CRC samples were downloaded from the TCGA database and analyzed, and differentially expressed lncRNA, miRNA and mRNA were screened by R program. The lncRNA-miRNA-mRNA ceRNA network in CRC was constructed by analyzing and integrating the relationships between differentially expressed RNAs through miRcode, TargetScan and miRTarbase databases.Kaplan-Meier method was used to analyze the relationship between the expression of lncRNA, miRNA, mRNA in ceRNA network and the survival prognosis of patients.Finally, the signal pathways involved in the occurrence and development of CRC were analyzed by GSEA functional enrichment analysis software. Results: A total of 614 differentially expressed lncRNAs, 244 differentially expressed miRNAs,and 12 672 differentially expressed mRNAs in CRC were identified; a ceRNA network consisting of 139 lncRNAs, 37 miRNAs and 228 mRNAs was constructed;It was found that 58 lncRNAs, 23 miRNAs, and 150 mRNAs were associated with the prognosis of CRC.The results of GSEA enrichment analysis showed that mRNA was mainly involved in signaling pathways such as Notch, Hedgehog and TGF-β. Conclusion: CRC-related ceRNA network was successfully constructed and lncRNAs, miRNAs and mRNAs associated with CRC prognosis were screened. It provides a valuable preliminary basis for further in-depth clinical research and basic experimental research on CRC.
2019, 26(10):1134-1141.
DOI: 10.3872/j.issn.1007-385X.2019.10.013
Abstract:
[Abstract] Objective: To investigate the mechanism of lncRNA XIST (XIST) on modulating gastric cancer progression via regulating miR-337-3p/HOXC8 axis. Methods: A total of 58 cases of gastric cancer tissues and corresponding para-cancerous tissues resected from March 2013 to January 2018 in Department of General Surgery, Kailuan General Hospital of Tangshan City were collected for this study; in addition, human gastric cancer cell lines (AGS, MGC803, HGC27) and human gastric mucosal GES-1 cells were also collected. qPCR was used to detect the expressions of XIST and miR-337-3p in above mentioned gastric tissues and cell lines. XIST-knockdown vectors, miR-337-3p mimics, miR-337-3p inhibitor and HOXC8-overexpression vectors were transfected into AGS cells. The proliferation and invasion of AGS cells were detected by CCK-8 and Transwell experiments respectively, and the expression levels of HOXC8, E-cadherin, N-cadherin and vimentin were detected by WB. The targeting relationships between XIST, miR-337-3p and HOXC8 were verified by dual-luciferase reporter gene assay. Results: XIST was up-regulated in gastric cancer tissues and cell lines (all P<0.01). XIST knockdown significantly inhibited proliferation, invasion and EMT of AGS cells (P<0.05 or P<0.01).Moreover, XIST directly interacted with miR-337-3p and down-regulated its expression, while HOXC8 was the target gene of miR-337-3p. Furthermore, XIST knockdown suppressed proliferation, invasion and EMT of AGS cells through up-regulating the inhibitory effect of miR-337-3p on HOXC8 (P<0.05 or P<0.01). Conclusion: XIST knockdown can suppress the proliferation, invasion and EMT of AGS cells, which may be related with down-regulation of HOXC8 by targeting miR-337-3p.
[Abstract] Objective: To investigate the mechanism of lncRNA XIST (XIST) on modulating gastric cancer progression via regulating miR-337-3p/HOXC8 axis. Methods: A total of 58 cases of gastric cancer tissues and corresponding para-cancerous tissues resected from March 2013 to January 2018 in Department of General Surgery, Kailuan General Hospital of Tangshan City were collected for this study; in addition, human gastric cancer cell lines (AGS, MGC803, HGC27) and human gastric mucosal GES-1 cells were also collected. qPCR was used to detect the expressions of XIST and miR-337-3p in above mentioned gastric tissues and cell lines. XIST-knockdown vectors, miR-337-3p mimics, miR-337-3p inhibitor and HOXC8-overexpression vectors were transfected into AGS cells. The proliferation and invasion of AGS cells were detected by CCK-8 and Transwell experiments respectively, and the expression levels of HOXC8, E-cadherin, N-cadherin and vimentin were detected by WB. The targeting relationships between XIST, miR-337-3p and HOXC8 were verified by dual-luciferase reporter gene assay. Results: XIST was up-regulated in gastric cancer tissues and cell lines (all P<0.01). XIST knockdown significantly inhibited proliferation, invasion and EMT of AGS cells (P<0.05 or P<0.01).Moreover, XIST directly interacted with miR-337-3p and down-regulated its expression, while HOXC8 was the target gene of miR-337-3p. Furthermore, XIST knockdown suppressed proliferation, invasion and EMT of AGS cells through up-regulating the inhibitory effect of miR-337-3p on HOXC8 (P<0.05 or P<0.01). Conclusion: XIST knockdown can suppress the proliferation, invasion and EMT of AGS cells, which may be related with down-regulation of HOXC8 by targeting miR-337-3p.
2019, 26(10):1142-1147.
DOI: 10.3872/j.issn.1007-385X.2019.10.014
Abstract:
[Abstract] Objective: To investigate the regulatory effect of miR-1297 on the malignant biological behaviors of breast cancer cells and its underlying mechanism. Methods: Twenty pairs of breast cancer tissues and para-cancer tissues resected at the Department of Thyroid and Breast Surgery of Leshan People ′ s Hospital from May 2016 to May 2018, as well as breast cancer cell lines MCF-7,SW626, HCC1937 and human breast epithelial MCF-10A cells were collected for this study. qPCR was performed to evaluate the expression of miR-1297 in breast cancer tissues and cell lines. The experimental cells were divided into control group, miR-1297 inhibitor group; TET3 over-expression group and simultaneous over-expression of TET3 and miR-1297 group. CCK-8 assay was used to detect the cell proliferation of MCF-7 cells; Transwell assay was carried out to detect the migration and invasion of MCF-7 cells; and WB was used to measure the expressions of TET3 and EMT related proteins (E-cadherin, N-cadherin and vimentin). Dual luciferase reporter gene assay was used to verify the relationship between miR-1297 and TET3. Results: miR-1297 was up-regulated in both breast cancer tissues and cell lines (P<0.01 or P<0.05). Knockdown of miR-1297 dramatically repressed the proliferation, migration, invasion and EMT of MCF-7 cells (P<0.01 or P<0.05). Over-expression of TET3 significantly up-regulated the expression of TET3 in MCF-7 cells (P<0.05). Simultaneous over-expression of TET3 and miR-1297 could reverse the expression level of TET3 in MCF-7 cells and the inhibitory effect of TET3 on the proliferation, migration, invasion and EMT of MCF-7 cells. Dual luciferase reporter gene assay results showed that miR-1297 targetedly bound to the 3' UTR of TET3. Further experiment results demonstrated that miR-1297 targetedly down-regulated TET3 and promoted the malignant biological behaviors of MCF-7 cells. Conclusion: miR-1297 is up-regulated in breast cancer tissues and cells; it promotes the malignant biological behaviors such as proliferation, migration, invasion and EMT through targetedly down-regulating the expression of TET3.
[Abstract] Objective: To investigate the regulatory effect of miR-1297 on the malignant biological behaviors of breast cancer cells and its underlying mechanism. Methods: Twenty pairs of breast cancer tissues and para-cancer tissues resected at the Department of Thyroid and Breast Surgery of Leshan People ′ s Hospital from May 2016 to May 2018, as well as breast cancer cell lines MCF-7,SW626, HCC1937 and human breast epithelial MCF-10A cells were collected for this study. qPCR was performed to evaluate the expression of miR-1297 in breast cancer tissues and cell lines. The experimental cells were divided into control group, miR-1297 inhibitor group; TET3 over-expression group and simultaneous over-expression of TET3 and miR-1297 group. CCK-8 assay was used to detect the cell proliferation of MCF-7 cells; Transwell assay was carried out to detect the migration and invasion of MCF-7 cells; and WB was used to measure the expressions of TET3 and EMT related proteins (E-cadherin, N-cadherin and vimentin). Dual luciferase reporter gene assay was used to verify the relationship between miR-1297 and TET3. Results: miR-1297 was up-regulated in both breast cancer tissues and cell lines (P<0.01 or P<0.05). Knockdown of miR-1297 dramatically repressed the proliferation, migration, invasion and EMT of MCF-7 cells (P<0.01 or P<0.05). Over-expression of TET3 significantly up-regulated the expression of TET3 in MCF-7 cells (P<0.05). Simultaneous over-expression of TET3 and miR-1297 could reverse the expression level of TET3 in MCF-7 cells and the inhibitory effect of TET3 on the proliferation, migration, invasion and EMT of MCF-7 cells. Dual luciferase reporter gene assay results showed that miR-1297 targetedly bound to the 3' UTR of TET3. Further experiment results demonstrated that miR-1297 targetedly down-regulated TET3 and promoted the malignant biological behaviors of MCF-7 cells. Conclusion: miR-1297 is up-regulated in breast cancer tissues and cells; it promotes the malignant biological behaviors such as proliferation, migration, invasion and EMT through targetedly down-regulating the expression of TET3.
2019, 26(10):1148-1155.
DOI: 10.3872/j.issn.1007-385X.2019.10.015
Abstract:
[摘要] 免疫治疗是继传统的手术、化疗、放疗和靶向治疗后的一种新兴的肿瘤治疗手段。以免疫检查点抑制剂（ICP）疗法为代表的免疫治疗在肿瘤临床治疗中取得了突破性进展。随着ICP 在临床的应用，用于肿瘤诊断、疗效及预后的生物标志物的探索也成为肿瘤免疫治疗研究的热点。在当前精准医疗的背景下，多项临床研究证实程序性死亡蛋白配体-1（PD-L1）表达、肿瘤突变负荷、微卫星不稳定以及肿瘤微环境相关的生物标志物与免疫治疗的疗效密切相关。然而，许多患者并不能从这些疗法中受益，缺乏有效的疗效和预后生物标志物在很大程度上限制了其临床应用。本文总结了有关免疫治疗生物标志物的相关研究文献，重点关注免疫治疗疗效和预后生物标志物在临床应用的相关研究进展，阐述可能有助于指导临床决策及治疗方案选择的潜在生物标志物。
[摘要] 免疫治疗是继传统的手术、化疗、放疗和靶向治疗后的一种新兴的肿瘤治疗手段。以免疫检查点抑制剂（ICP）疗法为代表的免疫治疗在肿瘤临床治疗中取得了突破性进展。随着ICP 在临床的应用，用于肿瘤诊断、疗效及预后的生物标志物的探索也成为肿瘤免疫治疗研究的热点。在当前精准医疗的背景下，多项临床研究证实程序性死亡蛋白配体-1（PD-L1）表达、肿瘤突变负荷、微卫星不稳定以及肿瘤微环境相关的生物标志物与免疫治疗的疗效密切相关。然而，许多患者并不能从这些疗法中受益，缺乏有效的疗效和预后生物标志物在很大程度上限制了其临床应用。本文总结了有关免疫治疗生物标志物的相关研究文献，重点关注免疫治疗疗效和预后生物标志物在临床应用的相关研究进展，阐述可能有助于指导临床决策及治疗方案选择的潜在生物标志物。
2019, 26(10):1156-1160.
DOI: 10.3872/j.issn.1007-385X.2019.10.016
Abstract:
[摘要] 肿瘤浸润性免疫细胞（TIC）参与构成肿瘤免疫微环境，调控肿瘤的生长，并影响患者的生存及抗肿瘤治疗的疗效。TIC分布模式的类型主要有冷肿瘤型、混合型和间质型。这3 种分布类型在免疫细胞的种类、数量与比例和分布位置上呈现明显的差别。在不同肿瘤、不同个体，甚至同一肿瘤的不同区域之间，TIC分布模式既有差异性也有规律性，既有模式相似但功能相异的差异性，也有模式不同但功能相近的规律性。TIC分布模式的分型体现的就是其差异性。近来研究发现，利用TIC分布模式可以预测患者的预后及抗肿瘤治疗的疗效，这体现的就是TIC分布模式的规律性。本文就该领域的研究进展进行综述。
[摘要] 肿瘤浸润性免疫细胞（TIC）参与构成肿瘤免疫微环境，调控肿瘤的生长，并影响患者的生存及抗肿瘤治疗的疗效。TIC分布模式的类型主要有冷肿瘤型、混合型和间质型。这3 种分布类型在免疫细胞的种类、数量与比例和分布位置上呈现明显的差别。在不同肿瘤、不同个体，甚至同一肿瘤的不同区域之间，TIC分布模式既有差异性也有规律性，既有模式相似但功能相异的差异性，也有模式不同但功能相近的规律性。TIC分布模式的分型体现的就是其差异性。近来研究发现，利用TIC分布模式可以预测患者的预后及抗肿瘤治疗的疗效，这体现的就是TIC分布模式的规律性。本文就该领域的研究进展进行综述。
2019, 26(10):1161-1166.
DOI: 10.3872/j.issn.1007-385X.2019.10.017
Abstract:
[摘要] CD47 是细胞表面高度糖化的穿膜蛋白，是一种“别吃我”信号，可与信号调节蛋白α（SIRPα）等形成CD47-SIRPα 抑制信号复合体，从固有免疫和适应性免疫两方面同时逃避机体的免疫监视。研究发现，CD47 在血液肿瘤和多种实体瘤中高表达，通过与巨噬细胞上的SIRPα 配体结合，启动一系列抑制性的信号转导而躲避吞噬，其高水平表达既能促进肿瘤细胞的生长又能促进肿瘤细胞的转移。通过抗CD47 抗体阻断CD47-SIRPα 信号通路，达到抑制肿瘤细胞的免疫逃逸，增强巨噬细胞的吞噬作用和适应性免疫应答，是免疫治疗肿瘤的新途径。目前，国内外开展了越来越多靶向CD47-SIRPα 的药物或抗体的基础研究和临床试验，有望从抗体分子设计和重组蛋白等方面解决靶向CD47 抗肿瘤治疗时发生的贫血和输液相关不良反应等问题。本文就CD47 的分子结构与生理功能、CD47-SIRPα 表达调控机制、CD47 抗肿瘤治疗研究现状以及靶向CD47 导致的相关生物安全性问题和解决方案等方面进行综述，为CD47新靶点的基础研究和临床应用提供参考。
[摘要] CD47 是细胞表面高度糖化的穿膜蛋白，是一种“别吃我”信号，可与信号调节蛋白α（SIRPα）等形成CD47-SIRPα 抑制信号复合体，从固有免疫和适应性免疫两方面同时逃避机体的免疫监视。研究发现，CD47 在血液肿瘤和多种实体瘤中高表达，通过与巨噬细胞上的SIRPα 配体结合，启动一系列抑制性的信号转导而躲避吞噬，其高水平表达既能促进肿瘤细胞的生长又能促进肿瘤细胞的转移。通过抗CD47 抗体阻断CD47-SIRPα 信号通路，达到抑制肿瘤细胞的免疫逃逸，增强巨噬细胞的吞噬作用和适应性免疫应答，是免疫治疗肿瘤的新途径。目前，国内外开展了越来越多靶向CD47-SIRPα 的药物或抗体的基础研究和临床试验，有望从抗体分子设计和重组蛋白等方面解决靶向CD47 抗肿瘤治疗时发生的贫血和输液相关不良反应等问题。本文就CD47 的分子结构与生理功能、CD47-SIRPα 表达调控机制、CD47 抗肿瘤治疗研究现状以及靶向CD47 导致的相关生物安全性问题和解决方案等方面进行综述，为CD47新靶点的基础研究和临床应用提供参考。
2019, 26(10):1167-1171.
DOI: 10.3872/j.issn.1007-385X.2019.10.018
Abstract:
[摘要] 非编码RNA（ncRNA）是一类不具有编码蛋白功能的RNA转录本，其异常表达参与了肿瘤的发生与发展。ncRNA的组织特异性表达使其具有鉴别肿瘤，甚至具有对肿瘤分型、分期的应用潜能。雌激素受体阴性（ER-）乳腺癌是指不表达ER的乳腺癌，其治疗困难、预后极差、病死率居乳腺癌之首。ncRNA在ER-乳腺癌中存在差异表达，并可通过参与非雌激素激活通路在乳腺癌的发生发展及预后过程中起重要调控作用。本文拟针对ncRNA中的微小RNA（miRNA）、长链非编码RNA（lncRNA）、环状RNA（circRNA）在ER-乳腺癌中的作用展开综述，分析它们在临床中的应用价值，为ER-乳腺癌的早期诊断及预后判断提供新的分子标志物和监测手段。
[摘要] 非编码RNA（ncRNA）是一类不具有编码蛋白功能的RNA转录本，其异常表达参与了肿瘤的发生与发展。ncRNA的组织特异性表达使其具有鉴别肿瘤，甚至具有对肿瘤分型、分期的应用潜能。雌激素受体阴性（ER-）乳腺癌是指不表达ER的乳腺癌，其治疗困难、预后极差、病死率居乳腺癌之首。ncRNA在ER-乳腺癌中存在差异表达，并可通过参与非雌激素激活通路在乳腺癌的发生发展及预后过程中起重要调控作用。本文拟针对ncRNA中的微小RNA（miRNA）、长链非编码RNA（lncRNA）、环状RNA（circRNA）在ER-乳腺癌中的作用展开综述，分析它们在临床中的应用价值，为ER-乳腺癌的早期诊断及预后判断提供新的分子标志物和监测手段。
19 Role of lncRNA/miRNA regulation axis in the occurrence and development of nasopharyngeal carcinoma
2019, 26(10):1172-1176.
DOI: 10.3872/j.issn.1007-385X.2019.10.019
Abstract:
[摘要] 长链非编码RNA（lncRNA）是一类长度超过200 个核苷酸的非蛋白质编码RNA，在表观遗传、转录和转录后水平调控各种生物学功能。微小RNA（miRNA）是一类长度为19~25 个核苷酸的小的非编码RNA，通过诱导mRNA降解或抑制其翻译，在转录后水平调控基因表达。多项研究显示，lncRNA和miRNA与鼻咽癌的发生发展密切相关，然而其潜在的分子机制尚未阐明。目前认为，lncRNA和miRNA之间的相互作用形成的lncRNA/miRNA轴可以通过调控某些经典信号转导途径或相关蛋白的表达参与鼻咽癌的发生发展。本文介绍了lncRNA/miRNA调控轴在鼻咽癌生长、转移和治疗中的作用及其机制，并初步总结了现阶段已知的鼻咽癌中lncRNA和miRNA相互作用调控网络。
[摘要] 长链非编码RNA（lncRNA）是一类长度超过200 个核苷酸的非蛋白质编码RNA，在表观遗传、转录和转录后水平调控各种生物学功能。微小RNA（miRNA）是一类长度为19~25 个核苷酸的小的非编码RNA，通过诱导mRNA降解或抑制其翻译，在转录后水平调控基因表达。多项研究显示，lncRNA和miRNA与鼻咽癌的发生发展密切相关，然而其潜在的分子机制尚未阐明。目前认为，lncRNA和miRNA之间的相互作用形成的lncRNA/miRNA轴可以通过调控某些经典信号转导途径或相关蛋白的表达参与鼻咽癌的发生发展。本文介绍了lncRNA/miRNA调控轴在鼻咽癌生长、转移和治疗中的作用及其机制，并初步总结了现阶段已知的鼻咽癌中lncRNA和miRNA相互作用调控网络。
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- 《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
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- 刊号：ISSN 1007-385X
- CN 31-1725/R
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.