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Volume 27,Issue 1,2020 Table of Contents
2020, 27(1):1-8.
DOI: 10.3872/j.issn.1007-385X.2020.01.001
Abstract:
Uncontrolled chronic inflammation plays key roles in the carcinogenesis of hepatocellular carcinoma (HCC). Among the risk factors of HCC, such as chronic viral hepatitis, alcoholic hepatitis, non-alcoholic steatohepatitis and so on, the occurrence and development of uncontrolled chronic inflammation are the core factors of HCC. The damaged or dead hepatocytes generated during the process of chronic inflammation may lead to the activation of immune cells in the liver, resulting in hepatic inflammation. Chronic and prolonged liver inflammation promotes the occurrence of cancer. During this process, different injuries or death patterns of hepatocytes and progression of inflammation caused by activation of different immune cells play different roles in hepatic carcinogenesis, involving multiple pathological or pathophysiological processes such as liver injury, inflammation, and compensatory proliferation, as well as function alteration of various cells, signaling pathways, and regulatory molecules. Further studies on the regulatory mechanisms of hepatic inflammation-induced carcinogenesis are helpful to provide theoretical basis for the intervention of occurrence of HCC. This review focused on the research progress of regulatory mechanisms involved in the hepatic inflammation-induced carcinogenesis.
Uncontrolled chronic inflammation plays key roles in the carcinogenesis of hepatocellular carcinoma (HCC). Among the risk factors of HCC, such as chronic viral hepatitis, alcoholic hepatitis, non-alcoholic steatohepatitis and so on, the occurrence and development of uncontrolled chronic inflammation are the core factors of HCC. The damaged or dead hepatocytes generated during the process of chronic inflammation may lead to the activation of immune cells in the liver, resulting in hepatic inflammation. Chronic and prolonged liver inflammation promotes the occurrence of cancer. During this process, different injuries or death patterns of hepatocytes and progression of inflammation caused by activation of different immune cells play different roles in hepatic carcinogenesis, involving multiple pathological or pathophysiological processes such as liver injury, inflammation, and compensatory proliferation, as well as function alteration of various cells, signaling pathways, and regulatory molecules. Further studies on the regulatory mechanisms of hepatic inflammation-induced carcinogenesis are helpful to provide theoretical basis for the intervention of occurrence of HCC. This review focused on the research progress of regulatory mechanisms involved in the hepatic inflammation-induced carcinogenesis.
2020, 27(1):9-18.
DOI: 10.3872/j.issn.1007-385X.2020.01.002
Abstract:
Objective:To investigate the effects of miR-200c on the proliferation, apoptosis and migration of triple negative breast cancer cell (TNBC) MDA-MB-231 and its metabolism-related molecular mechanism. Methods: miR-200c-231 (MDA-MB-231 over‐expressing miR-200c) cells, miR-NC-231 (MDA-MB-231 transfected with miRNA-negative control) and the corresponding transplant‐ed tumor models in nude mice were used as the study subjects. qPCR was used to detect the content of miR-200c and other related genes in cells and transplanted tumor tissues. The number of Ki67 positive cells in tumor tissue was analyzed by immunohistochemistry.The migration and apoptosis of cells were examined by Transwell chamber method and Flow cytometry, respectively. The expressions of proteins associated with proliferation, migration, and metabolism related signaling pathways in cells and tissues were confirmed by Western blotting. The changes of oxygen consumption rate (OCR), extracellular acidification rate (ECAR) and metabolic phenotype were detected by Seahorse energy metabolism detector. UPLC/LTQ-Orbitrap-MS technique was used to profile the difference of metabo‐lites in cells. Results: The content of miR-200c in miR-200c-231 cells was significantly higher than that in miR-NC-231 cells. The mass of miR-200c-231 transplanted tumor notably decreased, and the number of Ki67 positive cells in tumor tissues also decreased significantly.The migration ability of miR-200c-231 cells decreased and the apoptosis rate increased (all P<0.01), accompanied with declined expres‐sions of ZEB1/2, Vimentin, cyclin D1 and increased expression of cleaved PARP (P<0.05 or P<0.01), as well as decreased phosphorylation lever of STAT1/3 and NF-κB but incresed phosphorylation lever of CAMP(all P<0.05). Overexpression of miR-200c in MDA-MB-231 cells increased OCR and the content of 10 antitumor metabolites, but decreased ECAR and tryptophan 2,3-plus dioxidase (TDO2) expression (P<0.05 or P<0.01). Conclusion: miR-200c targeting TDO2 elevates the level of intracellular anticancer metabolites in TNBC MDAMB-231 cells, promotes the transformation from glycolysis to aerobic respiration phenotype, and inactivates STAT3 and NF-κB pathy‐way but activates cAMP pathway TNBC MDA-MB-231 cells, thus affects the malignant biological behaviors of MDA-MB-231 cells.
Objective:To investigate the effects of miR-200c on the proliferation, apoptosis and migration of triple negative breast cancer cell (TNBC) MDA-MB-231 and its metabolism-related molecular mechanism. Methods: miR-200c-231 (MDA-MB-231 over‐expressing miR-200c) cells, miR-NC-231 (MDA-MB-231 transfected with miRNA-negative control) and the corresponding transplant‐ed tumor models in nude mice were used as the study subjects. qPCR was used to detect the content of miR-200c and other related genes in cells and transplanted tumor tissues. The number of Ki67 positive cells in tumor tissue was analyzed by immunohistochemistry.The migration and apoptosis of cells were examined by Transwell chamber method and Flow cytometry, respectively. The expressions of proteins associated with proliferation, migration, and metabolism related signaling pathways in cells and tissues were confirmed by Western blotting. The changes of oxygen consumption rate (OCR), extracellular acidification rate (ECAR) and metabolic phenotype were detected by Seahorse energy metabolism detector. UPLC/LTQ-Orbitrap-MS technique was used to profile the difference of metabo‐lites in cells. Results: The content of miR-200c in miR-200c-231 cells was significantly higher than that in miR-NC-231 cells. The mass of miR-200c-231 transplanted tumor notably decreased, and the number of Ki67 positive cells in tumor tissues also decreased significantly.The migration ability of miR-200c-231 cells decreased and the apoptosis rate increased (all P<0.01), accompanied with declined expres‐sions of ZEB1/2, Vimentin, cyclin D1 and increased expression of cleaved PARP (P<0.05 or P<0.01), as well as decreased phosphorylation lever of STAT1/3 and NF-κB but incresed phosphorylation lever of CAMP(all P<0.05). Overexpression of miR-200c in MDA-MB-231 cells increased OCR and the content of 10 antitumor metabolites, but decreased ECAR and tryptophan 2,3-plus dioxidase (TDO2) expression (P<0.05 or P<0.01). Conclusion: miR-200c targeting TDO2 elevates the level of intracellular anticancer metabolites in TNBC MDAMB-231 cells, promotes the transformation from glycolysis to aerobic respiration phenotype, and inactivates STAT3 and NF-κB pathy‐way but activates cAMP pathway TNBC MDA-MB-231 cells, thus affects the malignant biological behaviors of MDA-MB-231 cells.
JIANG Ping
,
YANG Xike
,
WANG Qiuyu
,
SHAO Lanyun
,
WANG Songpeng
,
FANG Jianrui
,
FU Pengxiao
,
GUO Yingying
2020, 27(1):19-24.
DOI: 10.3872/j.issn.1007-385X.2020.01.003
Abstract:
Objective: To explore the action mechanism of miR-139-5p inhibiting proliferation and invasion of epithelial ovarian cancer (EOC) cells by targetedly regulating Notch1. Methods: A total of 24 pairs of EOC tissues and its corresponding para-cancerous tissues from patients, who underwent surgical resection in the Department of Gynecology, Nanyang Central Hospital of Henan Province,were collected for this study; in addition, human ovarian cancer cell lines (SKOV3, ES2, HEY-T30) and human ovarian epithelial cell line IOSE80 were also collected. Real-time quantitative PCR (qPCR) was applied to detect mRNAexpression of miR-139-5p and Notch1 in EOC tissues and cell lines. The miR-139-5p over-expression vector and recombinant plasmid pLV-Notch1 were transfected into SKOV3 cells. Blank control group (Ctrl group) and negative control group (NC group) were set up. Dual luciferase reporter gene assay was applied to verify the targeting relationship between miR-139-5p and Notch1 3'-UTR. CCK-8, Transwell and Scratch healing experi‐ments were applied to detect cell proliferation invasion and migration, respectively. Western blotting was applied to detect expressions of proliferation and migration related proteins in cells. Results: Compared with para-cancerous tissues and IOSE80 cells, the expression of miR-139-5p was significantly decreased in EOC tissues and cell lines, while the expression of Notch1 mRNA was significantly in‐creased (all P<0.01). The results of Dual luciferase reporter showed that Notch1 was the downstream target gene of miR-139-5p. Com‐pared with NC group, cell proliferation, invasion and migration ability, expression levels of Notch1, NICD, Cyclin D1, Cyclin A1,Snail1, β-catenin and N-cadherin were all significantly decreased on 3 d in miR-139-5p mimic group (all P<0.01), while expression of E-cadherin was significantly increased (P<0.01); meanwhile, over-expression of Notch1 could reverse the inhibitory effect of miR-139- 5p on proliferation, invasion and migration of SKOV3 cells. Conclusion: miR-139-5p can targetedly regulate Notch1 to inhibit prolifer‐ation, invasion and migration of EOC cells, which may be related to its down-regulation of NICD, Cyclin D1, Cyclin A1, Snail1, β-catenin and N-cadherin, and up-regulation of E-cadherin.
Objective: To explore the action mechanism of miR-139-5p inhibiting proliferation and invasion of epithelial ovarian cancer (EOC) cells by targetedly regulating Notch1. Methods: A total of 24 pairs of EOC tissues and its corresponding para-cancerous tissues from patients, who underwent surgical resection in the Department of Gynecology, Nanyang Central Hospital of Henan Province,were collected for this study; in addition, human ovarian cancer cell lines (SKOV3, ES2, HEY-T30) and human ovarian epithelial cell line IOSE80 were also collected. Real-time quantitative PCR (qPCR) was applied to detect mRNAexpression of miR-139-5p and Notch1 in EOC tissues and cell lines. The miR-139-5p over-expression vector and recombinant plasmid pLV-Notch1 were transfected into SKOV3 cells. Blank control group (Ctrl group) and negative control group (NC group) were set up. Dual luciferase reporter gene assay was applied to verify the targeting relationship between miR-139-5p and Notch1 3'-UTR. CCK-8, Transwell and Scratch healing experi‐ments were applied to detect cell proliferation invasion and migration, respectively. Western blotting was applied to detect expressions of proliferation and migration related proteins in cells. Results: Compared with para-cancerous tissues and IOSE80 cells, the expression of miR-139-5p was significantly decreased in EOC tissues and cell lines, while the expression of Notch1 mRNA was significantly in‐creased (all P<0.01). The results of Dual luciferase reporter showed that Notch1 was the downstream target gene of miR-139-5p. Com‐pared with NC group, cell proliferation, invasion and migration ability, expression levels of Notch1, NICD, Cyclin D1, Cyclin A1,Snail1, β-catenin and N-cadherin were all significantly decreased on 3 d in miR-139-5p mimic group (all P<0.01), while expression of E-cadherin was significantly increased (P<0.01); meanwhile, over-expression of Notch1 could reverse the inhibitory effect of miR-139- 5p on proliferation, invasion and migration of SKOV3 cells. Conclusion: miR-139-5p can targetedly regulate Notch1 to inhibit prolifer‐ation, invasion and migration of EOC cells, which may be related to its down-regulation of NICD, Cyclin D1, Cyclin A1, Snail1, β-catenin and N-cadherin, and up-regulation of E-cadherin.
2020, 27(1):25-30.
DOI: 10.3872/j.issn.1007-385X.2020.01.004
Abstract:
Objective: To investigate the effect of long non-coding RNA CDKN2B antisense RNA 1 (CDKN2B-AS1) on malignant biological behaviors of melanoma B16-F10 cells by targeting miR-7-5p. Methods: Melanoma B16-F10 cells were chosen for this study.shRNA CDKN2B-AS1 vector was constructed and transfected into B16-F10 cells. The experimental cells were divided into control group, sh-CDKN2B-AS1 group, miR-7-5p mimic group and miR-7-5p inhibitor group. The expression level of CDKN2B-AS1 mRNA in the transfected B16-F10 cells was detected by RT-PCR; the number of clone formation and the proliferation ability of the cells were detected by Clone formation assay and MTT assay; and the migration and invasion ability of the cells were detected by Scratch-healing assay and Transwell assay. The targeting relationship between CDKN2B-AS1 and miR-7-5p was detected by Luciferase reporter gene assay. The mRNA expression of miR-7-5p and protein expressions of Ki67, cleaved caspase-3, E-cadherin, N-cadherin and Twist1 in B16-F10 cells after transfection with miR-7-5p mimics/inhibitor were detected by RT-PCR and Western blotting, respectively. Results:Compared with the control group, the expression level of CDKN2B-AS1 mRNA in B16-F10 cells of sh-CDKN2B-AS1 group was significantly decreased (P<0.01); the proliferation, migration and invasion ability of cells were significantly decreased (all P<0.01).Luciferase reporter gene assay showed that CDKN2B-AS1 directly targeted miR-7-5p. The mRNA expression of miR-7-5p, and protein expressions of cleaved caspase-3 and E-cadherin in sh-CDKN2B-AS1 group and miR-7-5p mimic group were significantly up-regulated (all P<0.05), while the protein expressions of Ki67, N-cadherin, and Twist1 were significantly down-regulated (all P<0.05). Conclusion:CDKN2B-AS1 targets miR-7-5p to promote the development of melanoma, and interfering with CDKN2B-AS1 can inhibit the malig‐nant biological behaviors of melanoma B16-F10 cells.
Objective: To investigate the effect of long non-coding RNA CDKN2B antisense RNA 1 (CDKN2B-AS1) on malignant biological behaviors of melanoma B16-F10 cells by targeting miR-7-5p. Methods: Melanoma B16-F10 cells were chosen for this study.shRNA CDKN2B-AS1 vector was constructed and transfected into B16-F10 cells. The experimental cells were divided into control group, sh-CDKN2B-AS1 group, miR-7-5p mimic group and miR-7-5p inhibitor group. The expression level of CDKN2B-AS1 mRNA in the transfected B16-F10 cells was detected by RT-PCR; the number of clone formation and the proliferation ability of the cells were detected by Clone formation assay and MTT assay; and the migration and invasion ability of the cells were detected by Scratch-healing assay and Transwell assay. The targeting relationship between CDKN2B-AS1 and miR-7-5p was detected by Luciferase reporter gene assay. The mRNA expression of miR-7-5p and protein expressions of Ki67, cleaved caspase-3, E-cadherin, N-cadherin and Twist1 in B16-F10 cells after transfection with miR-7-5p mimics/inhibitor were detected by RT-PCR and Western blotting, respectively. Results:Compared with the control group, the expression level of CDKN2B-AS1 mRNA in B16-F10 cells of sh-CDKN2B-AS1 group was significantly decreased (P<0.01); the proliferation, migration and invasion ability of cells were significantly decreased (all P<0.01).Luciferase reporter gene assay showed that CDKN2B-AS1 directly targeted miR-7-5p. The mRNA expression of miR-7-5p, and protein expressions of cleaved caspase-3 and E-cadherin in sh-CDKN2B-AS1 group and miR-7-5p mimic group were significantly up-regulated (all P<0.05), while the protein expressions of Ki67, N-cadherin, and Twist1 were significantly down-regulated (all P<0.05). Conclusion:CDKN2B-AS1 targets miR-7-5p to promote the development of melanoma, and interfering with CDKN2B-AS1 can inhibit the malig‐nant biological behaviors of melanoma B16-F10 cells.
2020, 27(1):31-36.
DOI: 10.3872/j.issn.1007-385X.2020.01.005
Abstract:
Objective: To study the effects of vitamin C (VC) on reversing cisplatin (DDP) resistance in oral squamous cell carcinoma (OSCC) and the mechanism. Methods: Human OSCC CAL27 cells were cultured in vitro and DDP-resistant CAL27 cell line (CAL27/DDP) was screened by increasing concentration gradient method. Plate clone formation assay, CCK-8, Wound healing assay, Annexin V-FITC/PI staining flow cytometry were used to determine the effects of DDP alone or in combination with VC on colony formation,proliferation, migration and apoptosis of CAL27/DDP cells. Western blotting was used to detect the expression level of P-gp protein in CAL27 cells, CAL27/DDP cells and VC treated CAL27/DDP cells. Results: The inhibition concentration (IC50) of DDP increased significantly in CAL27/DDP cells as compared with that in CAL27 cells (P<0.05), indicating CAL27/DDP was DDP-resistant. After the combination with VC, the IC50 of DDP on CAL27/DDP cells was significantly reduced compared with that of DDP alone (P<0.05).DDP combined with VC significantly inhibited the migration of CAL27/DDP cells (P<0.01), and promoted the apoptosis rate (P<0.01).The expression level of P-gp protein in CAL27/DDP cells was increased compared with that in CAL27 cells (P<0.05), but decreased after VC intervention (P<0.05). Conclusion: VC can reverse DDP-resistance in OSCC cells by inhibiting P-gp protein expression.
Objective: To study the effects of vitamin C (VC) on reversing cisplatin (DDP) resistance in oral squamous cell carcinoma (OSCC) and the mechanism. Methods: Human OSCC CAL27 cells were cultured in vitro and DDP-resistant CAL27 cell line (CAL27/DDP) was screened by increasing concentration gradient method. Plate clone formation assay, CCK-8, Wound healing assay, Annexin V-FITC/PI staining flow cytometry were used to determine the effects of DDP alone or in combination with VC on colony formation,proliferation, migration and apoptosis of CAL27/DDP cells. Western blotting was used to detect the expression level of P-gp protein in CAL27 cells, CAL27/DDP cells and VC treated CAL27/DDP cells. Results: The inhibition concentration (IC50) of DDP increased significantly in CAL27/DDP cells as compared with that in CAL27 cells (P<0.05), indicating CAL27/DDP was DDP-resistant. After the combination with VC, the IC50 of DDP on CAL27/DDP cells was significantly reduced compared with that of DDP alone (P<0.05).DDP combined with VC significantly inhibited the migration of CAL27/DDP cells (P<0.01), and promoted the apoptosis rate (P<0.01).The expression level of P-gp protein in CAL27/DDP cells was increased compared with that in CAL27 cells (P<0.05), but decreased after VC intervention (P<0.05). Conclusion: VC can reverse DDP-resistance in OSCC cells by inhibiting P-gp protein expression.
6 Salidroside regulates DC through TLR4 to increase the lethality of T cells to lung cancer 3LL cells
2020, 27(1):37-41.
DOI: 10.3872/j.issn.1007-385X.2020.01.006
Abstract:
Objective：To investigate the effect of salidroside (SAL) on the phenotype of dendritic cells (DCs) and the antitumor ability of cytotoxic T lymphocytes (CTL). Methods：Lewis lung cancer cell line 3LL, wild type (WT) C57BL/6 mice and TLR4-/- C57BL/6 mice were chosen for this study. Mice bone marrow derived DC precursor cells were obtained to differentiate into immature DCs,which were harvested on the sixth day of culture. CD11c+ DCs were obtained by magnetic beads screening, and further divided into PBS group, SAL group and lipopolysaccharide (LPS) group. After being cultured for 48 h, the effects of SAL on surface molecules and phagocytosis of DCs as well as the efffect of TLR4 pathway on the killing effect of T cells were detected by Fow cytometry. Results：Compared with PBS group, expressions of DC surface molecules CD80, CD86 and MHC Ⅱ significantly increased (all P<0.05), phago‐cytosis significantly decreased (P<0.05), and TLR4 expression level significantly increased (P<0.01) in SAL group; Compared with WT group, after being treated with SAL or LPS, the expressions of DC surface molecules CD80, CD86 and MHC Ⅱ decreased signifi‐cantly in TLR4-/- group (all P<0.05); Compared with PBS group, the activated CTLin SAL group exhibited a significantly elevated killing effect against lung cancer 3LL cells (P<0.05). Conclusion：SAL can induce DC maturation by regulating TLR4, thus improving the kill‐ing ability of T cells.
Objective：To investigate the effect of salidroside (SAL) on the phenotype of dendritic cells (DCs) and the antitumor ability of cytotoxic T lymphocytes (CTL). Methods：Lewis lung cancer cell line 3LL, wild type (WT) C57BL/6 mice and TLR4-/- C57BL/6 mice were chosen for this study. Mice bone marrow derived DC precursor cells were obtained to differentiate into immature DCs,which were harvested on the sixth day of culture. CD11c+ DCs were obtained by magnetic beads screening, and further divided into PBS group, SAL group and lipopolysaccharide (LPS) group. After being cultured for 48 h, the effects of SAL on surface molecules and phagocytosis of DCs as well as the efffect of TLR4 pathway on the killing effect of T cells were detected by Fow cytometry. Results：Compared with PBS group, expressions of DC surface molecules CD80, CD86 and MHC Ⅱ significantly increased (all P<0.05), phago‐cytosis significantly decreased (P<0.05), and TLR4 expression level significantly increased (P<0.01) in SAL group; Compared with WT group, after being treated with SAL or LPS, the expressions of DC surface molecules CD80, CD86 and MHC Ⅱ decreased signifi‐cantly in TLR4-/- group (all P<0.05); Compared with PBS group, the activated CTLin SAL group exhibited a significantly elevated killing effect against lung cancer 3LL cells (P<0.05). Conclusion：SAL can induce DC maturation by regulating TLR4, thus improving the kill‐ing ability of T cells.
2020, 27(1):42-49.
DOI: 10.3872/j.issn.1007-385X.2020.01.007
Abstract:
Objective: To investigate the expression of tetraspanins-29 (Tspan29) in breast cancer tissues and cell lines and to explore the effect of Tspan29 knockdown on proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) of breast cancer MCF-7 and MDA-MB-231 cells. Methods: A total of 20 pairs of breast cancer tissues and corresponding para-cancerous tissues resected in Minhang Branch of Cancer Hospital Affiliated to Fudan University from June 2017 to February 2018 were collected for this study; in addition, breast cancer cell lines MCF-7, MDA-MB-231 and human breast epithelial MDA-kb2 cells were also collected. The mRNA and protein expressions of Tspan29 in above mentioned tissues and cell lines were detected by Real-time quantitative (qPCR) and Western blotting. The expression of Tspan29 in MCF-7 and MDA-MB-231 cells was interfered by siRNA. qPCR was used to detect the mRNA and protein expressions of Tspan29. PCR microarray was used to examine the expressions of EMT-related genes in MCF-7 cells.CCK-8 assay and Transwell were used to detect cell proliferation, migration and invasion of MCF-7 and MDA-MB-231 cells. Results:The mRNA and protein expressions of Tspan29 in breast cancer tissues were significantly higher than that in para-cancerous tissues (all P<0.01); and the mRNA and protein expressions of Tspan29 in MCF-7 and MDA-MB-231 cells were significantly higher than that in MDA-kb2 cells (P<0.01). After being interfered with siTspan29, the mRNA and protein expressions of Tspan29 were significantly down-regulated in MCF-7 cells (all P<0.05); the proliferation, invasion and migration of MCF-7 and MDA-MB-231 cells were signifi‐cantly inhibited (all P<0.05); and among the EMT-related genes, two were significantly up-regulated while 7 were down-regulated.Conclusion: Tspan29 is significantly up-regulated in breast cancer tissues and cell lines, and knockdown of Tspan29 significantly inhibits the proliferation, invasion and migration of breast cancer cells.
Objective: To investigate the expression of tetraspanins-29 (Tspan29) in breast cancer tissues and cell lines and to explore the effect of Tspan29 knockdown on proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) of breast cancer MCF-7 and MDA-MB-231 cells. Methods: A total of 20 pairs of breast cancer tissues and corresponding para-cancerous tissues resected in Minhang Branch of Cancer Hospital Affiliated to Fudan University from June 2017 to February 2018 were collected for this study; in addition, breast cancer cell lines MCF-7, MDA-MB-231 and human breast epithelial MDA-kb2 cells were also collected. The mRNA and protein expressions of Tspan29 in above mentioned tissues and cell lines were detected by Real-time quantitative (qPCR) and Western blotting. The expression of Tspan29 in MCF-7 and MDA-MB-231 cells was interfered by siRNA. qPCR was used to detect the mRNA and protein expressions of Tspan29. PCR microarray was used to examine the expressions of EMT-related genes in MCF-7 cells.CCK-8 assay and Transwell were used to detect cell proliferation, migration and invasion of MCF-7 and MDA-MB-231 cells. Results:The mRNA and protein expressions of Tspan29 in breast cancer tissues were significantly higher than that in para-cancerous tissues (all P<0.01); and the mRNA and protein expressions of Tspan29 in MCF-7 and MDA-MB-231 cells were significantly higher than that in MDA-kb2 cells (P<0.01). After being interfered with siTspan29, the mRNA and protein expressions of Tspan29 were significantly down-regulated in MCF-7 cells (all P<0.05); the proliferation, invasion and migration of MCF-7 and MDA-MB-231 cells were signifi‐cantly inhibited (all P<0.05); and among the EMT-related genes, two were significantly up-regulated while 7 were down-regulated.Conclusion: Tspan29 is significantly up-regulated in breast cancer tissues and cell lines, and knockdown of Tspan29 significantly inhibits the proliferation, invasion and migration of breast cancer cells.
2020, 27(1):50-54.
DOI: 10.3872/j.issn.1007-385X.2020.01.008
Abstract:
Objective: To investigate the effect of miR-361-5p on proliferation, invasion, migration, apoptosis and cell cycle of renal cell carcinoma ACHN cells. Methods: MiR-361-5p mimics and miR-361-5p inhibitor were transfected into ACHN cells, respectively.The expression of miR-361-5p in the transfected cells was detected by Real-time quantitatibse PCR; and the proliferation, migration,invasion, cell cycle and apoptosis of cells were detected by MTT assay, Scratch-healing assay, Transwell assay and flow cytometry,respectively. Results: Compared with the control group and mimics-NC group, the expression of miR-361-5p was increased significantly in ACHN cells of -miR-361-5p mimics group (P<0.01), the abilities of cell proliferation, invasion and migration were decreased significantly (all P<0.01), and the apoptosis rate was increased (P<0.01). Compared with the control group or inhibitor-NC group, the expression of miR-361-5p was significantly decreased in ACHN cells of miR-361-5p inhibitor group (P<0.01), the abilities of cell proliferation, invasion and migration were increased (all P<0.01), the cell cycle was accelerated (P<0.01), and the apoptosis rate was decreased (P<0.05). Conclusion: miR-361-5p can inhibit the proliferation, invasion and migration of renal cell carcinoma ACHN cells,and induce cell apoptosis, which plays an important inhibitory role in the development of renal cell carcinoma.
Objective: To investigate the effect of miR-361-5p on proliferation, invasion, migration, apoptosis and cell cycle of renal cell carcinoma ACHN cells. Methods: MiR-361-5p mimics and miR-361-5p inhibitor were transfected into ACHN cells, respectively.The expression of miR-361-5p in the transfected cells was detected by Real-time quantitatibse PCR; and the proliferation, migration,invasion, cell cycle and apoptosis of cells were detected by MTT assay, Scratch-healing assay, Transwell assay and flow cytometry,respectively. Results: Compared with the control group and mimics-NC group, the expression of miR-361-5p was increased significantly in ACHN cells of -miR-361-5p mimics group (P<0.01), the abilities of cell proliferation, invasion and migration were decreased significantly (all P<0.01), and the apoptosis rate was increased (P<0.01). Compared with the control group or inhibitor-NC group, the expression of miR-361-5p was significantly decreased in ACHN cells of miR-361-5p inhibitor group (P<0.01), the abilities of cell proliferation, invasion and migration were increased (all P<0.01), the cell cycle was accelerated (P<0.01), and the apoptosis rate was decreased (P<0.05). Conclusion: miR-361-5p can inhibit the proliferation, invasion and migration of renal cell carcinoma ACHN cells,and induce cell apoptosis, which plays an important inhibitory role in the development of renal cell carcinoma.
2020, 27(1):55-61.
DOI: 10.3872/j.issn.1007-385X.2020.01.009
Abstract:
Objective: To study the miR-28-3p expression in triple negative breast cancer (TNBC) tissues and cell lines, and explore its effect on the malignant biological behaviors of MDA-MB-468 cells. Methods：Tumor tissues and matched para-cancerous tissues were collected from 83 TNBC patients, who underwent tumor resection and pathological confirmation in the Fourth Hospital of Hebei Medical University between Jan. 2013 and Jan. 2014. TNBC cell lines (MDA-MB-468, HCC-1937, MDA-MB-231, MDA-MB-436, MDA-MB-453) and human normal breast epithelial cell line MCF10A were also used in this study. qPCR was used to detect the expression of miR-28-3p in above mentioned tissues and cell lines. The correlation between miR-28-3p expression and clinical parame‐ters was analyzed. After transfection with miR-28-3p inhibitor, the proliferation, apoptosis, invasion and migration ability of MDA-MB-468 cells were detected with CCK-8, Flow cytometry, Transwell and Wound-healing experiment, respectively. And Western blottingwas used to examine the protein expression of bridging integrator-1 (BIN1) in MDA-MB-468 cells. Bioinformatics BIN1 tool waere used to predict the target gene of miR-28-3p. Luciferase reporter gene assay was performed to validate the regulatory effect of miR-28-3p on BIN1. Results: The expression of miR-28-3p in TNBC tissues and cell lines was higher than that in matched para-cancerous tissues and MCF10A cells (all P<0.01), respectively. Among the total 83 TNBC tissues, 56 (67.47%) showed high miR-28-3p expression. High expression of miR-28-3p was closely correlated with the Ki-67 expression, tumor size and TNM stage (all P<0.05 or P<0.01). Compared with miR-NC group, transfection of miR-28-3p inhibitor significantly decreased the proliferation, invasion and mi‐gration of MDA-MB-468 cells while increased the apoptosis rate (all P<0.05 or P<0.01). Luciferase reporter gene assay confirmed that BIN1 was a target gene of miR-28-3p, and miR-28-3p inhibitor could up-regulate BIN1 expression in MDA-MB-468 cells (P<0.05).Conclusion: miR-28-3p is highly expressed in TNBC tissues and cell lines. miR-28-3p inhibitor up-regulates the expression of BIN1 to inhibit the proliferation, invasion and migration ability while promote the apoptosis of MDA-MB-468 cells.
Objective: To study the miR-28-3p expression in triple negative breast cancer (TNBC) tissues and cell lines, and explore its effect on the malignant biological behaviors of MDA-MB-468 cells. Methods：Tumor tissues and matched para-cancerous tissues were collected from 83 TNBC patients, who underwent tumor resection and pathological confirmation in the Fourth Hospital of Hebei Medical University between Jan. 2013 and Jan. 2014. TNBC cell lines (MDA-MB-468, HCC-1937, MDA-MB-231, MDA-MB-436, MDA-MB-453) and human normal breast epithelial cell line MCF10A were also used in this study. qPCR was used to detect the expression of miR-28-3p in above mentioned tissues and cell lines. The correlation between miR-28-3p expression and clinical parame‐ters was analyzed. After transfection with miR-28-3p inhibitor, the proliferation, apoptosis, invasion and migration ability of MDA-MB-468 cells were detected with CCK-8, Flow cytometry, Transwell and Wound-healing experiment, respectively. And Western blottingwas used to examine the protein expression of bridging integrator-1 (BIN1) in MDA-MB-468 cells. Bioinformatics BIN1 tool waere used to predict the target gene of miR-28-3p. Luciferase reporter gene assay was performed to validate the regulatory effect of miR-28-3p on BIN1. Results: The expression of miR-28-3p in TNBC tissues and cell lines was higher than that in matched para-cancerous tissues and MCF10A cells (all P<0.01), respectively. Among the total 83 TNBC tissues, 56 (67.47%) showed high miR-28-3p expression. High expression of miR-28-3p was closely correlated with the Ki-67 expression, tumor size and TNM stage (all P<0.05 or P<0.01). Compared with miR-NC group, transfection of miR-28-3p inhibitor significantly decreased the proliferation, invasion and mi‐gration of MDA-MB-468 cells while increased the apoptosis rate (all P<0.05 or P<0.01). Luciferase reporter gene assay confirmed that BIN1 was a target gene of miR-28-3p, and miR-28-3p inhibitor could up-regulate BIN1 expression in MDA-MB-468 cells (P<0.05).Conclusion: miR-28-3p is highly expressed in TNBC tissues and cell lines. miR-28-3p inhibitor up-regulates the expression of BIN1 to inhibit the proliferation, invasion and migration ability while promote the apoptosis of MDA-MB-468 cells.
2020, 27(1):62-67.
DOI: 10.3872/j.issn.1007-385X.2020.01.010
Abstract:
Objective: To investigate the expression of Artemin in chondrosarcoma and its effect on proliferation and migration of endothelial cells, and to explore the mechanism. Methods: A total of 40 chondrosarcoma tissue samples (low degree (Ⅰ), 20 cases; high degree (Ⅱ,Ⅲ), 20 cases) surgically resected from patients, who were treated in Lianyungang Hospital Affiliated to Nanjing University of Chinese Medicine from May, 2015 to April, 2019, were collected for this study. Another 20 cases of normal cartilage tissue specimen from patients with amputations due to car accidents were served as control. The expressions of Artemin, vascular endothelial growth factor (VEGF), Ki-67 and CD31+ vascular density in tumor tissues were detected by immunohistochemistry. After being treated with 10 ng/ml Artemin, the changes of VEGF, stromal cell derived factor-1 (SDF-1), matric metalloproteinase 2 (MMP2) and MMP9 in the su‐pernatant of SW1353 cell culture were detected by enzyme-linked immunosorbent assay (ELISA), and the effects of Artemin-treated chondrosarcoma cells on the migration and proliferation of ECV304 cells were detected by Transwell migration assay and MTT cell proliferation assay, respectively. Results: The expressions of Artemin and Ki-67 in the tissues of low-level group were significantly higher than those in the control group (all P<0.01); the expressions of Artemin and Ki-67 in the tissues of high-level group were signifi‐cantly higher than those in the low-level group (all P<0.01). The expression of Artemin was positively correlated with VEGF level and vascular density in chondrosarcoma tissues (all P<0.01); Artemin promoted the secretion of VEGF by chondrosarcoma cells, but had no significant effect on the secretion of SDF-1, MMP2 and MMP9. Artemin induced the proliferation and migration of ECV304 cells by promoting the secretion of VEGF by chondrosarcoma cells (all P<0.01). Conclusion: Artemin is highly expressed in chondrosarcoma tissues and has a positive correlation with the expression of VEGF and vascular density. Artemin can enhance the angiogenesis induced by chondrosarcoma.
Objective: To investigate the expression of Artemin in chondrosarcoma and its effect on proliferation and migration of endothelial cells, and to explore the mechanism. Methods: A total of 40 chondrosarcoma tissue samples (low degree (Ⅰ), 20 cases; high degree (Ⅱ,Ⅲ), 20 cases) surgically resected from patients, who were treated in Lianyungang Hospital Affiliated to Nanjing University of Chinese Medicine from May, 2015 to April, 2019, were collected for this study. Another 20 cases of normal cartilage tissue specimen from patients with amputations due to car accidents were served as control. The expressions of Artemin, vascular endothelial growth factor (VEGF), Ki-67 and CD31+ vascular density in tumor tissues were detected by immunohistochemistry. After being treated with 10 ng/ml Artemin, the changes of VEGF, stromal cell derived factor-1 (SDF-1), matric metalloproteinase 2 (MMP2) and MMP9 in the su‐pernatant of SW1353 cell culture were detected by enzyme-linked immunosorbent assay (ELISA), and the effects of Artemin-treated chondrosarcoma cells on the migration and proliferation of ECV304 cells were detected by Transwell migration assay and MTT cell proliferation assay, respectively. Results: The expressions of Artemin and Ki-67 in the tissues of low-level group were significantly higher than those in the control group (all P<0.01); the expressions of Artemin and Ki-67 in the tissues of high-level group were signifi‐cantly higher than those in the low-level group (all P<0.01). The expression of Artemin was positively correlated with VEGF level and vascular density in chondrosarcoma tissues (all P<0.01); Artemin promoted the secretion of VEGF by chondrosarcoma cells, but had no significant effect on the secretion of SDF-1, MMP2 and MMP9. Artemin induced the proliferation and migration of ECV304 cells by promoting the secretion of VEGF by chondrosarcoma cells (all P<0.01). Conclusion: Artemin is highly expressed in chondrosarcoma tissues and has a positive correlation with the expression of VEGF and vascular density. Artemin can enhance the angiogenesis induced by chondrosarcoma.
2020, 27(1):68-75.
DOI: 10.3872/j.issn.1007-385X.2020.01.011
Abstract:
弥漫大B细胞淋巴瘤（diffuse large B-cell lymphoma，DLBCL）是一种起源于B淋巴细胞的侵袭性恶性肿瘤，是世界上最常见的非霍奇金淋巴瘤。多种基因的遗传损伤引发B细胞内NF-κB信号通路持续性激活，促进B细胞恶性增殖，从而导致肿瘤生成。NF-κB信号通路的组成性激活在DLBCL的发病机制中起着重要作用，因此抑制NF-κB信号通路的过度激活成为DLB‐CL治疗研究的热点。近年来，多种NF-κB信号通路相关靶向抑制剂相继开发并进行临床试验。本文主要阐述DLBCL中B细胞受体和Toll样受体依赖性NF-κB信号通路异常激活的遗传学机制，及其在DLBCL发生和发展过程中的作用，并总结该信号通路靶向抑制剂的临床研究进展，旨在为DLBCL治疗方案的选择和靶向药物的开发提供参考依据
弥漫大B细胞淋巴瘤（diffuse large B-cell lymphoma，DLBCL）是一种起源于B淋巴细胞的侵袭性恶性肿瘤，是世界上最常见的非霍奇金淋巴瘤。多种基因的遗传损伤引发B细胞内NF-κB信号通路持续性激活，促进B细胞恶性增殖，从而导致肿瘤生成。NF-κB信号通路的组成性激活在DLBCL的发病机制中起着重要作用，因此抑制NF-κB信号通路的过度激活成为DLB‐CL治疗研究的热点。近年来，多种NF-κB信号通路相关靶向抑制剂相继开发并进行临床试验。本文主要阐述DLBCL中B细胞受体和Toll样受体依赖性NF-κB信号通路异常激活的遗传学机制，及其在DLBCL发生和发展过程中的作用，并总结该信号通路靶向抑制剂的临床研究进展，旨在为DLBCL治疗方案的选择和靶向药物的开发提供参考依据
2020, 27(1):76-81.
DOI: 10.3872/j.issn.1007-385X.2020.01.012
Abstract:
硒（Se）是一种在人体正常和肿瘤细胞的氧化还原反应进程中扮演重要角色和具有稳态调控因子作用的必需微量元素。流行病学和实验研究表明，Se对人体具有良好的保健作用；Se可能有助于阻滞肿瘤细胞分化的细胞系统的稳定，而Se化合物在肿瘤进程中的作用仍然具有争议。肿瘤干细胞（cancer stem cell，CSC）理论的出现，使得人们对于肿瘤诊治的认识发生了根本性的转变。虽然目前针对肿瘤的治疗方法是基于杀死大多数肿瘤细胞，但靶向CSC的治疗在提高治愈率方面具有很大的潜力。研究已证实，Se及其化合物在参与调控CSC的生物学行为中涉及许多信号转导通路，这也促使与CSC氧化还原和代谢调控的内在途径相关的高效、特异性强的Se及其化合物的深入研究。本文将对Se及其化合物调控CSC的氧化还原依赖的信号通路及自我更新、分化和迁移特性的主要基因调节位点进行总结，以提高肿瘤防治研究人员对于Se及其化合物对CSC作用的认识
硒（Se）是一种在人体正常和肿瘤细胞的氧化还原反应进程中扮演重要角色和具有稳态调控因子作用的必需微量元素。流行病学和实验研究表明，Se对人体具有良好的保健作用；Se可能有助于阻滞肿瘤细胞分化的细胞系统的稳定，而Se化合物在肿瘤进程中的作用仍然具有争议。肿瘤干细胞（cancer stem cell，CSC）理论的出现，使得人们对于肿瘤诊治的认识发生了根本性的转变。虽然目前针对肿瘤的治疗方法是基于杀死大多数肿瘤细胞，但靶向CSC的治疗在提高治愈率方面具有很大的潜力。研究已证实，Se及其化合物在参与调控CSC的生物学行为中涉及许多信号转导通路，这也促使与CSC氧化还原和代谢调控的内在途径相关的高效、特异性强的Se及其化合物的深入研究。本文将对Se及其化合物调控CSC的氧化还原依赖的信号通路及自我更新、分化和迁移特性的主要基因调节位点进行总结，以提高肿瘤防治研究人员对于Se及其化合物对CSC作用的认识
2020, 27(1):82-85.
DOI: 10.3872/j.issn.1007-385X.2020.01.013
Abstract:
外泌体是由细胞分泌的内含蛋白或核酸等活性物质、直径为35~120 nm的脂质双分子层囊泡。外泌体通过调控细胞间通讯，不仅参与调控细胞的正常生理过程，同时参与包括肿瘤在内的多种疾病的病理过程。肿瘤来源的外泌体参与肿瘤细胞与微环境的相互作用，并通过与转移、免疫抑制等相关信号通路刺激肿瘤的发生与发展。多发性骨髓瘤（multiple myeloma，MM）是最为常见的血液系恶性肿瘤之一，其具体发病机制尚未完全清楚，且缺乏安全、高效的诊疗手段。而外泌体因携带丰富的生物学信息，为肿瘤的治疗提供了一个新的靶点。因此，本文就外泌体在MM发生和发展中的作用及其以外泌体为基础的诊疗新方向作一综述。
外泌体是由细胞分泌的内含蛋白或核酸等活性物质、直径为35~120 nm的脂质双分子层囊泡。外泌体通过调控细胞间通讯，不仅参与调控细胞的正常生理过程，同时参与包括肿瘤在内的多种疾病的病理过程。肿瘤来源的外泌体参与肿瘤细胞与微环境的相互作用，并通过与转移、免疫抑制等相关信号通路刺激肿瘤的发生与发展。多发性骨髓瘤（multiple myeloma，MM）是最为常见的血液系恶性肿瘤之一，其具体发病机制尚未完全清楚，且缺乏安全、高效的诊疗手段。而外泌体因携带丰富的生物学信息，为肿瘤的治疗提供了一个新的靶点。因此，本文就外泌体在MM发生和发展中的作用及其以外泌体为基础的诊疗新方向作一综述。
2020, 27(1):86-90.
DOI: 10.3872/j.issn.1007-385X.2020.01.014
Abstract:
目前，针对肿瘤治疗药物在体内应用中的局限性，出现了许多高效的药物递送系统的研究，其中纳米药物载体技术和细胞药物载体技术较为热门，并取得了许多成果。纳米药物载体具有的优点，如防止药物发生降解及灭活，增加药物的靶向性，降低药物的毒副作用，可量产等。细胞载体更是利用细胞本身固有的特性，具有主动靶向肿瘤部位、低免疫原性和穿过体内生理屏障等优点，在药物递送研究中有广阔的应用前景，但是仍然存在很多问题及不足。研究人员创造性地将两者结合，使他们的优势互补，极大地强化了递送药的效率，增加了体内靶向性，降低了周围组织的细胞毒性等。本文从近几年来细胞-纳米药物载体系统研究的文献中，总结了红细胞、干细胞、单核/巨噬细胞、T细胞、树突状细胞（dendritic cell，DC）等作为纳米药物细胞载体的优缺点及目前的应用现状。
目前，针对肿瘤治疗药物在体内应用中的局限性，出现了许多高效的药物递送系统的研究，其中纳米药物载体技术和细胞药物载体技术较为热门，并取得了许多成果。纳米药物载体具有的优点，如防止药物发生降解及灭活，增加药物的靶向性，降低药物的毒副作用，可量产等。细胞载体更是利用细胞本身固有的特性，具有主动靶向肿瘤部位、低免疫原性和穿过体内生理屏障等优点，在药物递送研究中有广阔的应用前景，但是仍然存在很多问题及不足。研究人员创造性地将两者结合，使他们的优势互补，极大地强化了递送药的效率，增加了体内靶向性，降低了周围组织的细胞毒性等。本文从近几年来细胞-纳米药物载体系统研究的文献中，总结了红细胞、干细胞、单核/巨噬细胞、T细胞、树突状细胞（dendritic cell，DC）等作为纳米药物细胞载体的优缺点及目前的应用现状。
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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
- 邮编：200433
- 电话：021-81871002-22
- 电子邮箱：cjcb@biother.cn
- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.