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Volume 27,Issue 9,2020 Table of Contents
2020, 27(9):959-967.
DOI: 10.3872/j.issn.1007-385X.2020.09.001
Abstract:
T cell receptors (TCR) are specifically expressed on T cell surface, which can recognize different tumor antigens to kill and scavenge cancerous cells. TCR-engineered T cells (TCR-T) therapy is to harbor TCR specific to tumor cells and modify the T cells with genetic engineering techniques to achieve the purpose of treating tumors after transfusion. Despite some achievements in TCR-T therapy,there are still some problems, such as treatment toxicity, limited T cell infiltration and antigen-specific deficiency and so on. So, the safety and effectiveness of TCR-T therapy need to be constantly optimized. Therefore，this paper summarizes the research status of TCR-T therapy for solid tumors in domestic and overseas, as well as the existing problems and countermeasures.
T cell receptors (TCR) are specifically expressed on T cell surface, which can recognize different tumor antigens to kill and scavenge cancerous cells. TCR-engineered T cells (TCR-T) therapy is to harbor TCR specific to tumor cells and modify the T cells with genetic engineering techniques to achieve the purpose of treating tumors after transfusion. Despite some achievements in TCR-T therapy,there are still some problems, such as treatment toxicity, limited T cell infiltration and antigen-specific deficiency and so on. So, the safety and effectiveness of TCR-T therapy need to be constantly optimized. Therefore，this paper summarizes the research status of TCR-T therapy for solid tumors in domestic and overseas, as well as the existing problems and countermeasures.
2020, 27(9):968-977.
DOI: 10.3872/j.issn.1007-385X.2020.09.002
Abstract:
Objective: To investigate the effect of long non coding RNA (lncRNA) LINC00308 on proliferation, invasion and migration of prostate cancer cells and its related mechanism. Methods: lncRNAs and mRNAs differentially expressed in prostate cancer tissues and adjacent control tissues were screened by gene chip, and LINC00308 and TRIP13 (thyroid hormone receptor interactor13) were identified as the research objects. The effects of LINC00308 on the proliferation, invasion and migration of prostate cancer cells were detected by MTT assay, plate cloning, Transwell and scratch test. The above effects were verified in nude mice xenografts. The effect of LINC00308 on expression of TRIP13 in tumor tissues and cancer cells was detected by Western blotting and immunohistochemistry. Bioinformatics analysis, RIP (RNA immunoprecipitation), qPCR and Double luciferase gene reporter experi‐ments were used to predict and explore the interaction mechanism between miR-361-5p and LINC00308 as well as TRIP13, and plate cloning and Transwell invasion test were used to verify the biological behaviors of cancer cells. Results: Both the microarray results and qPCR confirmed that the expressions of LINC00308 (P<0.01) and TRIP13 (P<0.05) were abnormally high in prostate cancer tis‐sues and four cell lines; cell function test results showed that overexpression of LINC00308 could promote the proliferation, invasion and migration of prostate cancer PC3 cells (all P<0.05), while down-regulation of LINC00308 in prostate cancer cells had the opposite effect. In nude mice. LINC00308 could promote the tumorigenesis of prostate cancer cells in vivo, and increase the expression of TRIP13 both in vivo and in vitro (P<0.05). Bioinformatics analysis, RIP, qPCR and Double luciferase gene reporter results confirmed that miR-361-5p could bind to 3'-UTR of LINC00308 and TRIP13 respectively, and LINC00308 could act as a competing endogenous RNA (ceRNA) by sponging miR-361-5p to regulate the expression of TRIP13. In addition, MTT, plate cloning and Transwell assay confirmed the regulatory interaction among LINC00308 miR-361-5p and TRIP13 from the levels of proliferation, colony formation and invasion in cancer cells. Conclusion: LINC00308, which is abnormally highly expressed in prostate cancer tissues and cells, can inhibit the expression of miR-361-5p and enhance the expression of TRIP13 by exerting its ceRNA function, thus promoting the proliferation,invasion and migration of prostate cancer.
Objective: To investigate the effect of long non coding RNA (lncRNA) LINC00308 on proliferation, invasion and migration of prostate cancer cells and its related mechanism. Methods: lncRNAs and mRNAs differentially expressed in prostate cancer tissues and adjacent control tissues were screened by gene chip, and LINC00308 and TRIP13 (thyroid hormone receptor interactor13) were identified as the research objects. The effects of LINC00308 on the proliferation, invasion and migration of prostate cancer cells were detected by MTT assay, plate cloning, Transwell and scratch test. The above effects were verified in nude mice xenografts. The effect of LINC00308 on expression of TRIP13 in tumor tissues and cancer cells was detected by Western blotting and immunohistochemistry. Bioinformatics analysis, RIP (RNA immunoprecipitation), qPCR and Double luciferase gene reporter experi‐ments were used to predict and explore the interaction mechanism between miR-361-5p and LINC00308 as well as TRIP13, and plate cloning and Transwell invasion test were used to verify the biological behaviors of cancer cells. Results: Both the microarray results and qPCR confirmed that the expressions of LINC00308 (P<0.01) and TRIP13 (P<0.05) were abnormally high in prostate cancer tis‐sues and four cell lines; cell function test results showed that overexpression of LINC00308 could promote the proliferation, invasion and migration of prostate cancer PC3 cells (all P<0.05), while down-regulation of LINC00308 in prostate cancer cells had the opposite effect. In nude mice. LINC00308 could promote the tumorigenesis of prostate cancer cells in vivo, and increase the expression of TRIP13 both in vivo and in vitro (P<0.05). Bioinformatics analysis, RIP, qPCR and Double luciferase gene reporter results confirmed that miR-361-5p could bind to 3'-UTR of LINC00308 and TRIP13 respectively, and LINC00308 could act as a competing endogenous RNA (ceRNA) by sponging miR-361-5p to regulate the expression of TRIP13. In addition, MTT, plate cloning and Transwell assay confirmed the regulatory interaction among LINC00308 miR-361-5p and TRIP13 from the levels of proliferation, colony formation and invasion in cancer cells. Conclusion: LINC00308, which is abnormally highly expressed in prostate cancer tissues and cells, can inhibit the expression of miR-361-5p and enhance the expression of TRIP13 by exerting its ceRNA function, thus promoting the proliferation,invasion and migration of prostate cancer.
2020, 27(9):978-983.
DOI: 10.3872/j.issn.1007-385X.2020.09.003
Abstract:
Objective: To explore the regulatory effect of long non-coding RNA (lncRNA) SNHG5 on invasion and migration of hypoxia-induced hepatocellular carcinoma (HCC) cells. Methods: A total of 20 pairs of cancer and para-cancerous tissue specimens resected from HCC patients in the First Affiliated Hospital of Xi'an Jiaotong University from January 2017 to June 2018, and human HCC cell lines (HepG2, MHCC-97L, MHCC-97H , Huh7) as well as immortalized human liver LO2 cells were collected for this study.Bioinformatics methods were used to analyze the binding sites between hypoxia-inducible factor 1α (HIF-1α) and SNHG5. pCMVHIF-1α and shRNA-SNHG5 (sh-SNHG5) plasmids were transfected into HCC cells, respectively. qPCR was used to detect the expres‐sion level of SNHG5 in HCC tissues and hypoxia-induced HCC cells. Western botting was used to detect the expression level of HIF-1α protein in HCC cells, and Transwell chamber method was used to detect the migration and invasion ability of HCC cells after SNHG5 si‐lence under normoxia and hypoxia condition. Results: Compared with para-cancerous tissues and immortalized human liver LO2 cells,the expression of SNHG5 was significantly up-regulated in HCC tissues and cell lines (all P<0.01). Hypoxia promoted the expression level of SNHG5 in HCC cells, and its mechanism might be related to the combination of hypoxia-activated HIF-1α and SNHG5 promoter to promote its transcription. Hypoxia promoted the invasion and migration ability of HepG2 and MHCC-97L cells (all P<0.01), but knockdown of SNHG5 significantly inhibited the invasion and migration ability of HepG2 and MHCC-97L cells under hy‐poxic conditions (all P<0.01). Conclusion: SNHG5 is highly expressed in HCC tissues and cell lines and plays an important role in the invasion and migration of HCC cells induced by hypoxia.
Objective: To explore the regulatory effect of long non-coding RNA (lncRNA) SNHG5 on invasion and migration of hypoxia-induced hepatocellular carcinoma (HCC) cells. Methods: A total of 20 pairs of cancer and para-cancerous tissue specimens resected from HCC patients in the First Affiliated Hospital of Xi'an Jiaotong University from January 2017 to June 2018, and human HCC cell lines (HepG2, MHCC-97L, MHCC-97H , Huh7) as well as immortalized human liver LO2 cells were collected for this study.Bioinformatics methods were used to analyze the binding sites between hypoxia-inducible factor 1α (HIF-1α) and SNHG5. pCMVHIF-1α and shRNA-SNHG5 (sh-SNHG5) plasmids were transfected into HCC cells, respectively. qPCR was used to detect the expres‐sion level of SNHG5 in HCC tissues and hypoxia-induced HCC cells. Western botting was used to detect the expression level of HIF-1α protein in HCC cells, and Transwell chamber method was used to detect the migration and invasion ability of HCC cells after SNHG5 si‐lence under normoxia and hypoxia condition. Results: Compared with para-cancerous tissues and immortalized human liver LO2 cells,the expression of SNHG5 was significantly up-regulated in HCC tissues and cell lines (all P<0.01). Hypoxia promoted the expression level of SNHG5 in HCC cells, and its mechanism might be related to the combination of hypoxia-activated HIF-1α and SNHG5 promoter to promote its transcription. Hypoxia promoted the invasion and migration ability of HepG2 and MHCC-97L cells (all P<0.01), but knockdown of SNHG5 significantly inhibited the invasion and migration ability of HepG2 and MHCC-97L cells under hy‐poxic conditions (all P<0.01). Conclusion: SNHG5 is highly expressed in HCC tissues and cell lines and plays an important role in the invasion and migration of HCC cells induced by hypoxia.
2020, 27(9):984-991.
DOI: 10.3872/j.issn.1007-385X.2020.09.004
Abstract:
Objective: To investigate the molecular mechanism of microRNA-101 (miR-101) inhibiting the migration and invasion of non-small cell lung cancer (NSCLC) via targeting fibroblast growth factor 2 (FGF2). Methods: qPCR was used to detect the expression levels of miR-101 and FGF2 in human normal lung epithelial BEAS-2B cells and NSCLC cell lines (A549, H661 and SK-MES-1) as well as A549 cells after transfection. MiR-NC, miR-101 mimics, miR-IN-NC, miR-101 inhibitor or pcDNA-3.1 empty plasmid,pcDNA-FGF2 were respectively transfected into A549 cells. Wound healing assay and Transwell assay were used to examine the effects of overexpression of miR-101 and FGF2 on the migration and invasion of A549 cells. Western blotting(WB) was used to detect the expression levels of FGF2, E-cadherin, N-cadherin, Vimentin, ERK1/2 and p-ERK1/2 in A549 cells in each group. Results: The expression level of miR-101 in NSCLC cell lines were significantly lower than that in normal lung epithelial cells (all P<0.05), while the expression level in A549 cells was the lowest. Overexpression of miR-101 significantly inhibited the migration (P<0.05) and invasion (P<0.01) of A549 cells, increased the expression level of E-cadherin but decreased the expression level of Vimentin (P<0.05),N-cadherin (P<0.01) and p-ERK1/2 (P<0.05). Inhibition of miR-101 significantly enhanced the invasion and migration of A549 cells (all P<0.05), decreased the expression level of E-cadherin but increased the expression levels of Vimentin, N-cadherin and p-ERK1/2 (all P<0.05). The results of WB and Dual-luciferase reporter gene assay verified that FGF2 is a direct target gene of miR-101, and over‐expression of FGF2 significantly enhanced the invasion and migration of A549 cells (all P<0.01), decreased the expression of E-cad‐herin (P<0.01) but increased the expressions of Vimentin (P<0.01), N-cadherin (P<0.05) and p-ERK1/2 (P<0.01). Compared with the FGF2 overexpression alone group, co-overexpression of miR-101 and FGF2 significantly reduced the invasion and migration of A549 cells (all P<0.01), increased the expression of E-cadherin (P<0.01), and decreased the expressions of Vimentin (P<0.01), N-cadherin (P<0.05) and p-ERK1/2 (P<0.01). Conclusion: By targeting FGF2, miR-101 inhibits the invasion and migration of NSCLC cells through suppressing the epithelial-mesenchymal transition (EMT) and ERK signaling pathway.
Objective: To investigate the molecular mechanism of microRNA-101 (miR-101) inhibiting the migration and invasion of non-small cell lung cancer (NSCLC) via targeting fibroblast growth factor 2 (FGF2). Methods: qPCR was used to detect the expression levels of miR-101 and FGF2 in human normal lung epithelial BEAS-2B cells and NSCLC cell lines (A549, H661 and SK-MES-1) as well as A549 cells after transfection. MiR-NC, miR-101 mimics, miR-IN-NC, miR-101 inhibitor or pcDNA-3.1 empty plasmid,pcDNA-FGF2 were respectively transfected into A549 cells. Wound healing assay and Transwell assay were used to examine the effects of overexpression of miR-101 and FGF2 on the migration and invasion of A549 cells. Western blotting(WB) was used to detect the expression levels of FGF2, E-cadherin, N-cadherin, Vimentin, ERK1/2 and p-ERK1/2 in A549 cells in each group. Results: The expression level of miR-101 in NSCLC cell lines were significantly lower than that in normal lung epithelial cells (all P<0.05), while the expression level in A549 cells was the lowest. Overexpression of miR-101 significantly inhibited the migration (P<0.05) and invasion (P<0.01) of A549 cells, increased the expression level of E-cadherin but decreased the expression level of Vimentin (P<0.05),N-cadherin (P<0.01) and p-ERK1/2 (P<0.05). Inhibition of miR-101 significantly enhanced the invasion and migration of A549 cells (all P<0.05), decreased the expression level of E-cadherin but increased the expression levels of Vimentin, N-cadherin and p-ERK1/2 (all P<0.05). The results of WB and Dual-luciferase reporter gene assay verified that FGF2 is a direct target gene of miR-101, and over‐expression of FGF2 significantly enhanced the invasion and migration of A549 cells (all P<0.01), decreased the expression of E-cad‐herin (P<0.01) but increased the expressions of Vimentin (P<0.01), N-cadherin (P<0.05) and p-ERK1/2 (P<0.01). Compared with the FGF2 overexpression alone group, co-overexpression of miR-101 and FGF2 significantly reduced the invasion and migration of A549 cells (all P<0.01), increased the expression of E-cadherin (P<0.01), and decreased the expressions of Vimentin (P<0.01), N-cadherin (P<0.05) and p-ERK1/2 (P<0.01). Conclusion: By targeting FGF2, miR-101 inhibits the invasion and migration of NSCLC cells through suppressing the epithelial-mesenchymal transition (EMT) and ERK signaling pathway.
2020, 27(9):992-998.
DOI: 10.3872/j.issn.1007-385X.2020.09.005
Abstract:
Objective: To investigate the effect of lncRNA MAFG-AS1/ miR-11181-3p/GLG1 axis on cell migration, invasion and aerobic glycolysis of gastric cancer (GC) cells and its possible mechanism. Methods: AGS, a GC cell line with relatively high expression of MAFG-AS1, was selected as the study object. qPCR was used to detect RNA expression levels of MAFG-AS1,miR-11181-3p and GLG1. Transwell and glycolysis analysis were used to investigate cell migration, invasion and aerobic glycolysis.Bioinformatics analysis and Dual luciferase reporter gene assay were used to analyze the interaction among MAFG-AS1, miR-11181-3p and GLG1. Results: Knockdown of MAFG-AS1 significantly up-regulated miR-11181-3p and down-regulated GLG1 expression (both P<0.01), and significantly inhibited migration, invasion and aerobic glycolysis of GC cells (all P<0.01). Luciferase reporter gene assay confirmed that MAFG-AS1 competitively sponged miR-11181-3p (P<0.01). Inhibition of miR-11181-3p or overexpression of GLG1 partially reversed the inhibitory effect of MAFG-AS1 knockdown on GC cell migration, invasion, and aerobic glycolysis (all P<0.05 or P<0.01). Conclusion: MAFG-AS1 promotes cell migration, invasion and aerobic glycolysis of GC cells via miR-11181-3p/GLG1 axis, and may be a potential molecular target for GC diagnosis and therapy.
Objective: To investigate the effect of lncRNA MAFG-AS1/ miR-11181-3p/GLG1 axis on cell migration, invasion and aerobic glycolysis of gastric cancer (GC) cells and its possible mechanism. Methods: AGS, a GC cell line with relatively high expression of MAFG-AS1, was selected as the study object. qPCR was used to detect RNA expression levels of MAFG-AS1,miR-11181-3p and GLG1. Transwell and glycolysis analysis were used to investigate cell migration, invasion and aerobic glycolysis.Bioinformatics analysis and Dual luciferase reporter gene assay were used to analyze the interaction among MAFG-AS1, miR-11181-3p and GLG1. Results: Knockdown of MAFG-AS1 significantly up-regulated miR-11181-3p and down-regulated GLG1 expression (both P<0.01), and significantly inhibited migration, invasion and aerobic glycolysis of GC cells (all P<0.01). Luciferase reporter gene assay confirmed that MAFG-AS1 competitively sponged miR-11181-3p (P<0.01). Inhibition of miR-11181-3p or overexpression of GLG1 partially reversed the inhibitory effect of MAFG-AS1 knockdown on GC cell migration, invasion, and aerobic glycolysis (all P<0.05 or P<0.01). Conclusion: MAFG-AS1 promotes cell migration, invasion and aerobic glycolysis of GC cells via miR-11181-3p/GLG1 axis, and may be a potential molecular target for GC diagnosis and therapy.
2020, 27(9):999-1005.
DOI: 10.3872/j.issn.1007-385X.2020.09.006
Abstract:
Objective: To study the effect of microRNA-141(miR-141) expression regulation on cell proliferation, cell cycle, apopto‐sis, invasion and migration of human prostate cancer cell line DU145 and its mechanism. Methods: MiR-141 mimics (miR-141 up group) and miR-141 inhibitors (miR-141 down group) were transfected into human prostate cancer DU145 cells by using liposome lipo‐fectamine 2000, and the un-transfection group (Control group) and non-sense miRNA sequence transfection group (NC group) were set.The expression of miRNA-141 in DU145 cells in each group before and after transfection was detected by qPCR. MTT assay was used to detect the proliferation viability and sensitivity to cisplatin (DDP) in DU145 cells of each group. Cell cycle and apoptosis rate of DU145 cells under DDP treatment were detected by Flow cytometry; the changes in cell invasion and migration ability were detected by Transwell method. The protein expressions of VEGF and EGFR in DU145 cells of each group were detected by Western blotting.Results: Compared with the Control and NC group, the level of miRNA-141 expression in the miR-141-down group decreased to (0.18±0.08), the cell proliferation viability decreased significantly while its sensitivity to DDP increased significantly, the cell cycle was blocked in the G0+G1 phase, and the apoptosis rate significantly increased to (46.67±5.86)% while cell invasion rate and migration rate significantly decreased to (44.34±8.32)%, (57.73±6.19)%, and the relative expression levels of VEGF and EGFR decreased to (0.47±0.06), (0.36±0.06), (P<0.05 or P<0.01). But in the miR-141-up group, the level of miRNA-141 expression increased to (4.23±0.53), the cell proliferation viability significantly increased while its sensitivity to DDP decreased significantly, and the cell cycle was promoted into S and G2 phase, the apoptosis rate significantly decreased to (18.77±4.24)% while cell invasion and migration rate significantly in‐creased to (89.94±6.34)%, (94.44±5.84)%, and the relative expression levels of VEGF and EGFR were up to (0.89±0.07), (0.73±0.06),(P<0.05 or P<0.01). Conclusion: miR-141 can act as a growth promoting factor in prostate cancer DU145 cells. miR-141 down-regula‐tion can significantly inhibit the proliferation viability, cell cycle, migration and invasion of DU145 cells, and promote cell apoptosis and DDP-sensitivity, and the mechanism of which may be related with inhibition of VEGF and EGFR protein expressions.
Objective: To study the effect of microRNA-141(miR-141) expression regulation on cell proliferation, cell cycle, apopto‐sis, invasion and migration of human prostate cancer cell line DU145 and its mechanism. Methods: MiR-141 mimics (miR-141 up group) and miR-141 inhibitors (miR-141 down group) were transfected into human prostate cancer DU145 cells by using liposome lipo‐fectamine 2000, and the un-transfection group (Control group) and non-sense miRNA sequence transfection group (NC group) were set.The expression of miRNA-141 in DU145 cells in each group before and after transfection was detected by qPCR. MTT assay was used to detect the proliferation viability and sensitivity to cisplatin (DDP) in DU145 cells of each group. Cell cycle and apoptosis rate of DU145 cells under DDP treatment were detected by Flow cytometry; the changes in cell invasion and migration ability were detected by Transwell method. The protein expressions of VEGF and EGFR in DU145 cells of each group were detected by Western blotting.Results: Compared with the Control and NC group, the level of miRNA-141 expression in the miR-141-down group decreased to (0.18±0.08), the cell proliferation viability decreased significantly while its sensitivity to DDP increased significantly, the cell cycle was blocked in the G0+G1 phase, and the apoptosis rate significantly increased to (46.67±5.86)% while cell invasion rate and migration rate significantly decreased to (44.34±8.32)%, (57.73±6.19)%, and the relative expression levels of VEGF and EGFR decreased to (0.47±0.06), (0.36±0.06), (P<0.05 or P<0.01). But in the miR-141-up group, the level of miRNA-141 expression increased to (4.23±0.53), the cell proliferation viability significantly increased while its sensitivity to DDP decreased significantly, and the cell cycle was promoted into S and G2 phase, the apoptosis rate significantly decreased to (18.77±4.24)% while cell invasion and migration rate significantly in‐creased to (89.94±6.34)%, (94.44±5.84)%, and the relative expression levels of VEGF and EGFR were up to (0.89±0.07), (0.73±0.06),(P<0.05 or P<0.01). Conclusion: miR-141 can act as a growth promoting factor in prostate cancer DU145 cells. miR-141 down-regula‐tion can significantly inhibit the proliferation viability, cell cycle, migration and invasion of DU145 cells, and promote cell apoptosis and DDP-sensitivity, and the mechanism of which may be related with inhibition of VEGF and EGFR protein expressions.
2020, 27(9):1006-1011.
DOI: 10.3872/j.issn.1007-385X.2020.09.007
Abstract:
Objective: To investigate the effect of long non-coding RNA DiGeorge syndrome critical region gene 5 (DGCR5) on proliferation, invasion and migration of esophageal squamous cell carcinoma (ESCC) TE1 cells and its mechanism. Methods: qPCR was used to detect the expression level of DGCR5 in ESCC cell lines (TE1, Yes-2, KYSE150 and Eca9706). TE1 cells were transfected with siRNA-DGCR5(si-DGCR5) and negative control (si-NC) plasmids, respectively. CCK-8, Wound healing and Transwell assay were used to detect the proliferation, migration and invasion of TE1 cells before and after DGCR5 knockdown. The relationship between DGCR5 expression and epidermal growth factor receptor (EGFR) in ESCC tissues was analyzed by GEPIA database. The mRNA and protein expressions of EGFR in ESCC cell line were examined by qPCR and Western blotting (WB). WB was further used to detect the expression of EGFR protein in TE1 cells before and after DGCR5 knockdown. Results: lncRNA DGCR5 was highly expressed in ESCC cell lines (all P<0.01). qPCR confirmed that the expression of DGCR5 in TE1 cells of si-DGCR5 group was significantly lower than that of si-NC group (P<0.01). The proliferation, migration and invasion ability of TE1 cells in si-DGCR5 group were significantly lower than those in si-NC group (all P<0.01). GEPIA database showed that the expression of DGCR5 was positively correlated with EGFR in ESCC tissues (P<0.01). WB showed that the protein level of EGFR in TE1 cells of si-DGCR5 group decreased significantly (P<0.01). Conclusion: lncRNA DGCR5 is highly expressed in ESCC cells, and promotes the proliferation, invasion and migration of TE1 cells possibly by up-regulating EGFR expression.
Objective: To investigate the effect of long non-coding RNA DiGeorge syndrome critical region gene 5 (DGCR5) on proliferation, invasion and migration of esophageal squamous cell carcinoma (ESCC) TE1 cells and its mechanism. Methods: qPCR was used to detect the expression level of DGCR5 in ESCC cell lines (TE1, Yes-2, KYSE150 and Eca9706). TE1 cells were transfected with siRNA-DGCR5(si-DGCR5) and negative control (si-NC) plasmids, respectively. CCK-8, Wound healing and Transwell assay were used to detect the proliferation, migration and invasion of TE1 cells before and after DGCR5 knockdown. The relationship between DGCR5 expression and epidermal growth factor receptor (EGFR) in ESCC tissues was analyzed by GEPIA database. The mRNA and protein expressions of EGFR in ESCC cell line were examined by qPCR and Western blotting (WB). WB was further used to detect the expression of EGFR protein in TE1 cells before and after DGCR5 knockdown. Results: lncRNA DGCR5 was highly expressed in ESCC cell lines (all P<0.01). qPCR confirmed that the expression of DGCR5 in TE1 cells of si-DGCR5 group was significantly lower than that of si-NC group (P<0.01). The proliferation, migration and invasion ability of TE1 cells in si-DGCR5 group were significantly lower than those in si-NC group (all P<0.01). GEPIA database showed that the expression of DGCR5 was positively correlated with EGFR in ESCC tissues (P<0.01). WB showed that the protein level of EGFR in TE1 cells of si-DGCR5 group decreased significantly (P<0.01). Conclusion: lncRNA DGCR5 is highly expressed in ESCC cells, and promotes the proliferation, invasion and migration of TE1 cells possibly by up-regulating EGFR expression.
2020, 27(9):1012-1017.
DOI: 10.3872/j.issn.1007-385X.2020.09.008
Abstract:
Objective: To construct a circRNA profile of esophageal squamous cell carcinoma (ESCC) and analyze differentially expressed circRNAs. Methods: Samples were taken from 3 patients with esophageal squamous cell carcinoma who were hospitalized in the Department of Thoracic Surgery, Jintan Hospital, Jiangsu University from June 2018 to February 2019. The circRNA expression profile was constructed by high-throughput sequencing technique, and the circRNA differentially expressed in 3 pairs of esophageal squamous cell carcinoma tissues and adjacent tissues was detected. The biological functions and related signal pathways of these circRNA were analyzed by GO and KEGG techniques. Results: By comparing the expression levels of circRNA between esophageal squamous cell carcinoma and adjacent tissues, 905 differentially expressed circRNA were found, of which 404 were up-regulated and 501 were down-regulated. hsa_circ_0004390 was the CIRC RNA with the highest up-regulation factor (FC=7.9712), and novel_circ_0012687 was the one with the highest down-regulation factor. GO and KEGG analysis showed that these circRNA may be involved in biological processes such as cell cycle, cell components and protein binding of cancer cells, and signal pathways such as Hippo and cGMP-PKG. Conclusion: The expression profile analysis of circRNA in esophageal squamous cell carcinoma showed that the signifi‐cantly differentially expressed circRNA could be used as a potential biomarker of esophageal squamous cell carcinoma.
Objective: To construct a circRNA profile of esophageal squamous cell carcinoma (ESCC) and analyze differentially expressed circRNAs. Methods: Samples were taken from 3 patients with esophageal squamous cell carcinoma who were hospitalized in the Department of Thoracic Surgery, Jintan Hospital, Jiangsu University from June 2018 to February 2019. The circRNA expression profile was constructed by high-throughput sequencing technique, and the circRNA differentially expressed in 3 pairs of esophageal squamous cell carcinoma tissues and adjacent tissues was detected. The biological functions and related signal pathways of these circRNA were analyzed by GO and KEGG techniques. Results: By comparing the expression levels of circRNA between esophageal squamous cell carcinoma and adjacent tissues, 905 differentially expressed circRNA were found, of which 404 were up-regulated and 501 were down-regulated. hsa_circ_0004390 was the CIRC RNA with the highest up-regulation factor (FC=7.9712), and novel_circ_0012687 was the one with the highest down-regulation factor. GO and KEGG analysis showed that these circRNA may be involved in biological processes such as cell cycle, cell components and protein binding of cancer cells, and signal pathways such as Hippo and cGMP-PKG. Conclusion: The expression profile analysis of circRNA in esophageal squamous cell carcinoma showed that the signifi‐cantly differentially expressed circRNA could be used as a potential biomarker of esophageal squamous cell carcinoma.
2020, 27(9):1018-1023.
DOI: 10.3872/j.issn.1007-385X.2020.09.009
Abstract:
Objective: To observe the effect of allogeneic platelets transfusion on the invasion and metastasis of human lung cancer A549 cells, and to preliminarily explore its mechanism of action. Methods: Eighty-nine patients with advanced lung cancer, who had received platelet transfusion in the Chemotherapy Department of Fourth Hospital of Hebei Medical University between January 2017 and December 2018, were enrolled in this study. The study cells were randomized into Ctrl group (A549 cells co-incubated with culture medium), Before group, and After group (A549 cells co-incubated with plasma Before and After platelet transfusion, respectively). The migration and invasion of A549 cells co-cultured with plasma before and after platelet transfection were detected by Scratch and Transwell experiments. The expression of MMPs, TIMPs and epithelial-mesenchymal transition (EMT) related proteins E-cadherin,N-cadherin and Vimentin, as well as vascular endothelial growth factor (VEGF) and its receptor 2 (VEGFR2) were detected by Western blotting (WB) method. Results: The scratch healing ability of A549 cells in After group was significantly higher than that of Ctrl group and Before group [(73.67±2.60)% vs (58.33±2.33)%, (35.33±2.03) %; P<0.01, vs Ctrl group; P<0.05, vs Before group], and there was also a significant difference between Before group and Ctrl group (P<0.05). The results of cell migration experiment showed that the number of transmembrane cells in After group was significantly higher than that in Ctrl group and Before group [(69.67±7.84) vs (18±2.08) and (39.33±2.03), all P<0.01]. The cell invasion experiment showed that the number of transmembrane cells in After group was significantly higher than that in Ctrl group and Before group [(59.34±3.46) vs (18.34±1.56) and (37.58±2.79), all P<0.01].When A549 cells were co-incubated with plasma before and after platelet transfusion for 48 h, it was found that the expressions of MMP9 and MMP2 were increased (P<0.05), while their inhibitors TIMP1 and TIMP2 were decreased (P<0.01); the expressions of EMT-related proteins N-cadherin and Vimentin were increased (P<0.05), but E-cadherin was decreased (P<0.01); the expressions of angiogenesis related proteins VEGF and VEGFR2 were increased (P<0.05). Conclusion: Alloplatelets transfusion can promote the invasion and metastasis of lung cancer A549 cells, which may be realized by regulation of the expressions of EMT, metallomatrix protease and vascular growth factor-related proteins.
Objective: To observe the effect of allogeneic platelets transfusion on the invasion and metastasis of human lung cancer A549 cells, and to preliminarily explore its mechanism of action. Methods: Eighty-nine patients with advanced lung cancer, who had received platelet transfusion in the Chemotherapy Department of Fourth Hospital of Hebei Medical University between January 2017 and December 2018, were enrolled in this study. The study cells were randomized into Ctrl group (A549 cells co-incubated with culture medium), Before group, and After group (A549 cells co-incubated with plasma Before and After platelet transfusion, respectively). The migration and invasion of A549 cells co-cultured with plasma before and after platelet transfection were detected by Scratch and Transwell experiments. The expression of MMPs, TIMPs and epithelial-mesenchymal transition (EMT) related proteins E-cadherin,N-cadherin and Vimentin, as well as vascular endothelial growth factor (VEGF) and its receptor 2 (VEGFR2) were detected by Western blotting (WB) method. Results: The scratch healing ability of A549 cells in After group was significantly higher than that of Ctrl group and Before group [(73.67±2.60)% vs (58.33±2.33)%, (35.33±2.03) %; P<0.01, vs Ctrl group; P<0.05, vs Before group], and there was also a significant difference between Before group and Ctrl group (P<0.05). The results of cell migration experiment showed that the number of transmembrane cells in After group was significantly higher than that in Ctrl group and Before group [(69.67±7.84) vs (18±2.08) and (39.33±2.03), all P<0.01]. The cell invasion experiment showed that the number of transmembrane cells in After group was significantly higher than that in Ctrl group and Before group [(59.34±3.46) vs (18.34±1.56) and (37.58±2.79), all P<0.01].When A549 cells were co-incubated with plasma before and after platelet transfusion for 48 h, it was found that the expressions of MMP9 and MMP2 were increased (P<0.05), while their inhibitors TIMP1 and TIMP2 were decreased (P<0.01); the expressions of EMT-related proteins N-cadherin and Vimentin were increased (P<0.05), but E-cadherin was decreased (P<0.01); the expressions of angiogenesis related proteins VEGF and VEGFR2 were increased (P<0.05). Conclusion: Alloplatelets transfusion can promote the invasion and metastasis of lung cancer A549 cells, which may be realized by regulation of the expressions of EMT, metallomatrix protease and vascular growth factor-related proteins.
2020, 27(9):1024-1029.
DOI: 10.3872/j.issn.1007-385X.2020.09.010
Abstract:
Objective: To investigate the effect of miR-383-5p on the proliferation and invasion of medulloblastoma (MB) by targeting DNA mismatch repair MSH6 gene. Methods: A total of 15 pairs of tumor tissues and corresponding adjacent tissues from MB patients,who were surgically treated and pathologically confirmed in the Department of Oncology of the Second Affiliated Hospital of Hainan Medical College from July 2014 to May 2017, were collected for this study. qPCR was applied to detect the expression of miR-383-5p in MB tissues and cell lines. The experimental cells were divided into control group (NC group), miR-383-3p overexpression group (miR-383-5p group), MSH6 knockdown group (si-MSH6 group) and miR-383-5p inhibitor+si-MSH6 group. CCK-8 assay was used to detect the proliferation of UW473 cells. Transwell assay was used to examine the invasion and migration of UW473 cells, the targeting relationship between miR-383-5p and MSH6 was verified by Dual-luciferase reporter gene assay, and Western blotting (WB) was performed to detect the protein expression of MSH6. Results: The expression level of miR-383-5p was significantly down-regulated in MB tissues and cell lines compared with para-cancer tissues (all P<0.05 or P<0.01). Overexpression of miR-383-5p significantly in‐hibited the proliferation, migration and invasion of UW473 cells (all P<0.05 or P<0.01), and down-regulated the expression level of MSH6 (all P<0.01). Dual-luciferase reporter gene assay demonstrated that miR-383-5p could targetedly bind to the 3'UTR of MSH6.Knockdown of MSH6 could inhibit the proliferation, invasion and migration of UW473 cells (all P<0.01). Further experiments showed that simultaneous knockdown of miR-383-5p and MSH6 could attenuate the inhibition of MSH6 silence on the proliferation, invasion and migration of UW473 cells. Conclusion: miR-383-5p expression is down-regulated in MB tissues and cell lines, and miR-383-5p suppresses the proliferation, migration and invasion of UW473 cells via targetedly down-regulating MSH6.
Objective: To investigate the effect of miR-383-5p on the proliferation and invasion of medulloblastoma (MB) by targeting DNA mismatch repair MSH6 gene. Methods: A total of 15 pairs of tumor tissues and corresponding adjacent tissues from MB patients,who were surgically treated and pathologically confirmed in the Department of Oncology of the Second Affiliated Hospital of Hainan Medical College from July 2014 to May 2017, were collected for this study. qPCR was applied to detect the expression of miR-383-5p in MB tissues and cell lines. The experimental cells were divided into control group (NC group), miR-383-3p overexpression group (miR-383-5p group), MSH6 knockdown group (si-MSH6 group) and miR-383-5p inhibitor+si-MSH6 group. CCK-8 assay was used to detect the proliferation of UW473 cells. Transwell assay was used to examine the invasion and migration of UW473 cells, the targeting relationship between miR-383-5p and MSH6 was verified by Dual-luciferase reporter gene assay, and Western blotting (WB) was performed to detect the protein expression of MSH6. Results: The expression level of miR-383-5p was significantly down-regulated in MB tissues and cell lines compared with para-cancer tissues (all P<0.05 or P<0.01). Overexpression of miR-383-5p significantly in‐hibited the proliferation, migration and invasion of UW473 cells (all P<0.05 or P<0.01), and down-regulated the expression level of MSH6 (all P<0.01). Dual-luciferase reporter gene assay demonstrated that miR-383-5p could targetedly bind to the 3'UTR of MSH6.Knockdown of MSH6 could inhibit the proliferation, invasion and migration of UW473 cells (all P<0.01). Further experiments showed that simultaneous knockdown of miR-383-5p and MSH6 could attenuate the inhibition of MSH6 silence on the proliferation, invasion and migration of UW473 cells. Conclusion: miR-383-5p expression is down-regulated in MB tissues and cell lines, and miR-383-5p suppresses the proliferation, migration and invasion of UW473 cells via targetedly down-regulating MSH6.
2020, 27(9):1030-1035.
DOI: 10.3872/j.issn.1007-385X.2020.09.011
Abstract:
Objective: To investigate the effect of long non-coding LINC00969 on proliferation and invasion of breast cancer cell.Methods: Real-time Quantitative polymerase chain reaction (qPCR) was used to detect differential expression of LINC00969 in five breast cancer cell lines (MCF-7, BT-20, MAD-MB-231, ZR-75-1, and SKBR3) , normal breast cells MCF-10A, and in 42 cases breast cancer tissues and adjacent tissues. TMCF-7 cells were transfected with LINC00969 plasmid and empty vector vector vector. The trans‐fection efficiency was verified by qPCR. CCK-8, plate cloning and edu assay were used to detect cell proliferation. Flow cytometry was used to detect cell cycle. Western blotting was used to detect PCNA, CyclinD1, MMP2 and MMP9. Scratch repair test and Transwell test were used to detect cell migration and invasion. Results：Compared with the adjacent tissues, LINC00969 expression in breast can‐cer tissues was significantly decreased (P<0.05); compared with breast cancer cells MCF-10A, LINC00969 expression in five breast cancer cells was significantly decreased (P<0.05), and the lowest was in MCF-7 cells; overexpression of LINC00969 significantly inhib‐ited the proliferation, colony formation and DNA synthesis of MCF-7 cells (all P<0.05), making MCF-7 cell cycle clear.The ability of wound healing, migration and invasion of the cells were significantly reduced (P<0.05). Overexpression of LINC00969 significantly in‐hibited the expression of PCNA, cyclinD1, MMP2 and MMP9 (all P<0.05). Conclusion: LINC00969 is low expressed in breast cancer.Overexpression of LINC00969 can inhibit proliferation and migration of breast cancer cell,the mechanism may be related to the abnor‐mal expression of cell cycle and migration related proteins.
Objective: To investigate the effect of long non-coding LINC00969 on proliferation and invasion of breast cancer cell.Methods: Real-time Quantitative polymerase chain reaction (qPCR) was used to detect differential expression of LINC00969 in five breast cancer cell lines (MCF-7, BT-20, MAD-MB-231, ZR-75-1, and SKBR3) , normal breast cells MCF-10A, and in 42 cases breast cancer tissues and adjacent tissues. TMCF-7 cells were transfected with LINC00969 plasmid and empty vector vector vector. The trans‐fection efficiency was verified by qPCR. CCK-8, plate cloning and edu assay were used to detect cell proliferation. Flow cytometry was used to detect cell cycle. Western blotting was used to detect PCNA, CyclinD1, MMP2 and MMP9. Scratch repair test and Transwell test were used to detect cell migration and invasion. Results：Compared with the adjacent tissues, LINC00969 expression in breast can‐cer tissues was significantly decreased (P<0.05); compared with breast cancer cells MCF-10A, LINC00969 expression in five breast cancer cells was significantly decreased (P<0.05), and the lowest was in MCF-7 cells; overexpression of LINC00969 significantly inhib‐ited the proliferation, colony formation and DNA synthesis of MCF-7 cells (all P<0.05), making MCF-7 cell cycle clear.The ability of wound healing, migration and invasion of the cells were significantly reduced (P<0.05). Overexpression of LINC00969 significantly in‐hibited the expression of PCNA, cyclinD1, MMP2 and MMP9 (all P<0.05). Conclusion: LINC00969 is low expressed in breast cancer.Overexpression of LINC00969 can inhibit proliferation and migration of breast cancer cell,the mechanism may be related to the abnor‐mal expression of cell cycle and migration related proteins.
2020, 27(9):1036-1042.
DOI: 10.3872/j.issn.1007-385X.2020.09.012
Abstract:
作为胞质中的 DNA 感受器，环腺苷酸鸟苷酸合成酶（cyclic GMP-AMP synthase，cGAS）能够识别细胞质内的异常DNA，激活干扰素刺激基因（stimulator of interferon genes，STING）信号通路，介导下游的干扰素相关基因、炎性相关因子和趋化因子的产生，从而启动机体的免疫应答。STING蛋白作为DNA感受通路下游关键的接头分子，广泛表达于免疫细胞、肿瘤细胞和基质细胞等多种类型的细胞中，发挥感受胞质DNA和免疫防御的信号转导作用。STING蛋白激动剂作为新型激动剂已用于多种肿瘤的临床前研究和临床试验治疗，展示出诱人的应用前景。但是，也有文献报道该信号通路的过度激活在某些情况下对肿瘤的生长有一定的促进作用。本文对近年来cGAS-STING信号通路调控免疫应答以及STING激动剂在肿瘤免疫治疗中应用的相关研究进展作一综述，为靶向该通路的抗肿瘤免疫治疗的临床应用提供依据。
作为胞质中的 DNA 感受器，环腺苷酸鸟苷酸合成酶（cyclic GMP-AMP synthase，cGAS）能够识别细胞质内的异常DNA，激活干扰素刺激基因（stimulator of interferon genes，STING）信号通路，介导下游的干扰素相关基因、炎性相关因子和趋化因子的产生，从而启动机体的免疫应答。STING蛋白作为DNA感受通路下游关键的接头分子，广泛表达于免疫细胞、肿瘤细胞和基质细胞等多种类型的细胞中，发挥感受胞质DNA和免疫防御的信号转导作用。STING蛋白激动剂作为新型激动剂已用于多种肿瘤的临床前研究和临床试验治疗，展示出诱人的应用前景。但是，也有文献报道该信号通路的过度激活在某些情况下对肿瘤的生长有一定的促进作用。本文对近年来cGAS-STING信号通路调控免疫应答以及STING激动剂在肿瘤免疫治疗中应用的相关研究进展作一综述，为靶向该通路的抗肿瘤免疫治疗的临床应用提供依据。
2020, 27(9):1043-1049.
DOI: 10.3872/j.issn.1007-385X.2020.09.013
Abstract:
局限期食管鳞状细胞癌的治疗推荐手术、放疗和化疗为主的综合治疗，晚期食管鳞癌则仍以化疗为主要手段，但多年来疗效一直徘徊不前，各种分子靶向药物治疗食管鳞癌的Ⅲ期临床研究亦多以失败告终。近年来，免疫治疗在食管鳞癌领域已显示出令人鼓舞的疗效和发展前景。本文综述了食管鳞癌免疫治疗的相关临床热点，包括肿瘤疫苗、过继性免疫细胞疗法和免疫检查点抑制剂在食管鳞癌治疗中的研究进展。
局限期食管鳞状细胞癌的治疗推荐手术、放疗和化疗为主的综合治疗，晚期食管鳞癌则仍以化疗为主要手段，但多年来疗效一直徘徊不前，各种分子靶向药物治疗食管鳞癌的Ⅲ期临床研究亦多以失败告终。近年来，免疫治疗在食管鳞癌领域已显示出令人鼓舞的疗效和发展前景。本文综述了食管鳞癌免疫治疗的相关临床热点，包括肿瘤疫苗、过继性免疫细胞疗法和免疫检查点抑制剂在食管鳞癌治疗中的研究进展。
2020, 27(9):1050-1055.
DOI: 10.3872/j.issn.1007-385X.2020.09.014
Abstract:
卵巢癌是妇科三大恶性肿瘤之一，由于早期患者自身无不适症状且对其缺乏可靠的诊断方法，加之目前对晚期卵巢癌患者缺乏有效的监测及治疗方法，故卵巢癌患者的病死率较高。肿瘤患者血液中的肿瘤源性外泌体（tumor-derived exosome,TEX）携带有与原肿瘤细胞一致的生物信息学特性，通过检测TEX可以无创、连续、实时监测肿瘤的发生发展情况，是卵巢癌早期诊断、治疗评估、预后随访潜在的有益指标。本文就TEX来源性质、在肿瘤微环境中的作用机制、目前分离鉴定技术及其在卵巢癌诊断治疗中应用的研究进展作一综述。
卵巢癌是妇科三大恶性肿瘤之一，由于早期患者自身无不适症状且对其缺乏可靠的诊断方法，加之目前对晚期卵巢癌患者缺乏有效的监测及治疗方法，故卵巢癌患者的病死率较高。肿瘤患者血液中的肿瘤源性外泌体（tumor-derived exosome,TEX）携带有与原肿瘤细胞一致的生物信息学特性，通过检测TEX可以无创、连续、实时监测肿瘤的发生发展情况，是卵巢癌早期诊断、治疗评估、预后随访潜在的有益指标。本文就TEX来源性质、在肿瘤微环境中的作用机制、目前分离鉴定技术及其在卵巢癌诊断治疗中应用的研究进展作一综述。
2020, 27(9):1056-1061.
DOI: 10.3872/j.issn.1007-385X.2020.09.015
Abstract:
肝细胞癌具有高发病率和高病死率的特点，在治疗过程中易发生复发或转移，目前缺乏高敏感度的生物标志物进行预测和评估。研究发现，循环肿瘤细胞可作为肝细胞癌潜在的生物标志物，能应用于肝细胞癌的早预测、早诊断、早治疗及治疗过程中的疾病监测，有助于预防和控制相关治疗的不良反应。本文将对循环肿瘤细胞作为生物标志物在肝细胞癌临床诊疗中应用的最新研究进展进行综述。
肝细胞癌具有高发病率和高病死率的特点，在治疗过程中易发生复发或转移，目前缺乏高敏感度的生物标志物进行预测和评估。研究发现，循环肿瘤细胞可作为肝细胞癌潜在的生物标志物，能应用于肝细胞癌的早预测、早诊断、早治疗及治疗过程中的疾病监测，有助于预防和控制相关治疗的不良反应。本文将对循环肿瘤细胞作为生物标志物在肝细胞癌临床诊疗中应用的最新研究进展进行综述。
2020, 27(9):1062-1067.
DOI: 10.3872/j.issn.1007-385X.2020.09.016
Abstract:
lncRNA XIST是在哺乳动物中发现最早的lncRNAs之一，尤其是在X染色体失活相关疾病中起着重要作用，在胃癌、肝细胞癌、结直肠癌、胰腺癌、膀胱癌、骨肉瘤、鼻咽癌、食管鳞状细胞癌等非生殖系统相关恶性肿瘤中，其作为癌基因通过介导ceRNA调控网络，促进肿瘤细胞的增殖、迁移、侵袭和耐药等生物学行为。本文就 lncRNA XIST的分子生物学属性及介导的ceRNA调控网络在多种恶性肿瘤中作用的研究进展作一综述，以期为后续的肿瘤防治研究提供新的方向。
lncRNA XIST是在哺乳动物中发现最早的lncRNAs之一，尤其是在X染色体失活相关疾病中起着重要作用，在胃癌、肝细胞癌、结直肠癌、胰腺癌、膀胱癌、骨肉瘤、鼻咽癌、食管鳞状细胞癌等非生殖系统相关恶性肿瘤中，其作为癌基因通过介导ceRNA调控网络，促进肿瘤细胞的增殖、迁移、侵袭和耐药等生物学行为。本文就 lncRNA XIST的分子生物学属性及介导的ceRNA调控网络在多种恶性肿瘤中作用的研究进展作一综述，以期为后续的肿瘤防治研究提供新的方向。
2020, 27(9):1068-1069.
DOI: 10.3872/j.issn.1007-385X.2020.09.017
Abstract:
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.