Mechanism Of MiR-125b Inhibiting Proliferation Of Esophageal Squamous Carcinoma Cells And Inducing Apoptosis

Purposes:To investigate the role of microRNA-125b(miR-125b)in the proliferation and apoptosis of esophageal squamous cell carcinoma(ESCC).The regulatory relationship between miR-125b and the candidate target bcl-2 modification factor(BMF)was clarified.To explore the significance of miR-125b/BMF pathway in the diagnosis of esophageal cancer.Materials and Methods:1.According to the research requirements,66 cases of ESCC cancer tissues and corresponding adjacent tissues were selected.Real-time quantitative PCR(qRT-PCR)was used to detect the expression level of miR-125b in tissues,and the correlation analysis was analyzed with clinical pathological data and prognosis.2.The expression of miR-125b in human esophageal cancer cell 109(EC 109)and human esophageal cancer cell 9706(EC9706)esophageal cancer cell lines and normal esophageal epithelial cells was examined.3.The synthetic miR-125b negative control(NC)or miR-125b mimetic or the corresponding inhibitor was transfected into the EC 109 and EC9706 esophageal cancer cell lines,and the miR-125b mimic and the cell count Kit-8(CCK8)were used to detect Changes that occur after the inhibitor is transfected into the ESCC cell line.Flow cytometry was used to detect changes in cell cycle and apoptosis after transfection.4.In vitro experiments to verify the role of miR-125b in ESCC,EC 109 cells were transfected into miR-125b mimics and NC and injected into nude mice,pay attention to observe their changes,regular weighing,pay attention to tumor block changes,understand Growth Status.According to the results,the tumor volume growth curve and the body mass curve were drawn.The volume and weight of tumor mass and the expression of Ki-67 in tumor tissues were detected by histology and immunohistochemistry.5.Find potential target genes for miR-125b through bioinformatics software Target Scan.BMF was identified as a candidate target gene.6.EC 109 and EC9706 cells were transfected with silencing BMF(si-BMF),BMF expression was detected by qRT-PCR and western blot,and cell proliferation was detected by CCK-8.BMF silencing and apoptosis were analyzed by Western blot.Relationship.The expression of BMF in ESCC patient tissues and ESCC cell lines was evaluated,and the relationship between miR-125b and BMF levels was analyzed.Results:1.In ESCC cancer tissues and cell lines,miR-125b expression was significantly reduced,and the decrease in miR-125b was significantly associated with lymphatic metastasis in patients.2.Overexpression of MiR-125b significantly inhibited cell growth,induced apoptosis,and increased the G1 phase of human esophageal cancer cell 109 and human esophageal cancer cell line 9706.3.Overexpression of miR-125b significantly inhibited tumor growth in vivo.4.BMF is a functional target for miR-125b to regulate proliferation,apoptosis and cell cycle of human esophageal cancer cells 109 and human esophageal cancer cells 9706.Conclusion:1.MiR-125b is significantly down-regulated in ESCC and has the diagnostic potential to become a lymph node metastasis in ESCC.2.MiR-125b significantly inhibits the proliferation of esophageal squamous carcinoma cells and induces apoptosis by targeting BMF.