RESUMEN
Objective To investigate the expression of sex determining region Y box protein 4(SOX4) gene and its biological effects in endometrial carcinoma. Methods 156 cases of endometrial carcinoma tissues, adjacent tissues of endometrial carcinoma and 156 cases of endometrial atypical hyperplasia were collected; Immunohistochemistry was used to detect the expression of SOX4 in endometrial cancer, endometrial dysplasia and normal endometrial tissue, and to analyze the relationship between SOX4 and the clinical characteristics of patients with endometrial cancer. After establishing the SOX4 overexpression/silencing Ishikawa cell strain using the lentivirus transfection technique, MTT, flow cytometry and Transwell chamber method were used to detect the cell proliferation, apoptosis, migration and invasion ability, and Western blotting method was used to detect SOX4, β-catenin and E-cadherin protein expression changes. Results The expression of SOX4 in endometrial cancer tissue was higher than that in normal endometrial tissue and endometrial atypical hyperplasia (P<0.05). SOX4 expression was correlated with invasion depth, International Federation of Obstetrics and Gynecoogy (FIGO) stage and lymph node metastasis (P<0.05). Compared with control group, SOX4 overexpressed Ishikawa cells have significantly increased proliferative ability, migration and invasion ability, significantly reduced apoptosis rate, significantly increased SOX4 and β-catenin protein expression, and significantly reduced E-cadherin protein expression (all P< 0.05). while the proliferation ability, migration and invasion ability of Ishikawa cells interfered by SOX4 were significantly reduced, the apoptosis rate was significantly increased, the expression of SOX4 and β-catenin protein was significantly reduced, and the expression of E-cadherin protein was significantly increased (all P<0.05). Conclusion S0X4 gene is highly expressed in endometrial cancer tissues, which may promote the development of endometrial cancer by activating Wnt/β-catenin signaling pathway.
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Objective To verify whether miR-630 could inhibit MDA-MB-231 cells migration and invasion by targeting Sox4 in triple-negative breast cancer(TNBC).Methods Collection normal breast tissue and breast cancer tissue from patients undergoing breast cancer resection.RT-PCR were used to test the expression of miR-630,miR-21,miR-195,miR-134,miR-200a,miR-381 and miR-1228.Western blot were used to test the expression of COL1A1,COL1 A5,MMP-2,MMP-9 and Sox4.In vitro experiment,after miR-630 was transfected into MDA-MB-231 cells,wound healing were employed to test the migratory ability of MDA-MB-231 cells,and transwell were used to test the invasion ability of MDA-MB-231 cells.Western blot were used to investigate the expressions of COL1 Al,COL1 A5,MMP-2,MMP-9 and Sox4 in MDA-MB-231 cell.Luciferase assay was used to confirmed whether Sox43'-UTR the target gene of miR-630.Results Compared with normal breast tissue,the expression of miR-630 was decreased(P＜0.01),meanwhile the expression of COL1A1,COL1A5,MMP-2,MMP-9 and Sox4 were significantly increased in the triple-negative breast cancer tissue(P＜0.01).In the vitro experiment,compared with the control group,the expression of COL1A1,COL1A5,MMP-2,MMP-9 and Sox4 were decreased in the miR-630 group (P＜0.05);The migration activity of MDA-MB-231 cells was decreased in the miR-630 group (P＜0.01);The Luciferase activity of the Sox4-3'-UTR plasmid was significantly suppressed by miR630 (P＜0.05);Over expression of Sox4 could reverse the effect of miR-630 on MDA-MB-231(P＜0.05,P＜0.01).Conclusion In triple-negative breast cancer tissue,the expression of miR-630 decreased;miR-630 inhibits triple-negative breast cancer cells migration and invasion by targeting Sox4-3’-UTR.