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Objective To investigate the effect of microRNA(miR)-4645-5p on the proliferation,invasion and epithelial-mesenchymal transition of esophageal cancer cells by targeting mucin 16(MUC16)and its mo-lecular mechanism.Methods The expression of miR-4645-5p in esophageal cancer tissues was analyzed online by TCGA database.The expression level of miR-4645-5p in esophageal cancer cell lines was analyzed by fluo-rescent real-time fluorescence quantitative polymerase chain reaction(qPCR).KYSE-30 cells were transfected with miR-4645-5p mimic and negative control mimic by lipofection technology,and were divided into miR-4645-5p group and control mimic group.The proliferation ability,migration ability and invasion ability of transfected KYSE-30 cells were analyzed by CCK-8 method,scratch test and Transwell test respectively.The target gene of miR-4645-5p was predicted by the bioinformatics website,and the binding of miR-4645-5p to the target gene was detected by the dual-luciferase reporter gene assay.The expression level of MUC16 mR-NA was detected by qPCR,and the protein expression levels of MUC16,transcription factor-1(ZEB-1),zonal atresia protein(ZO-1),tight junction protein-1(Claudin-1)and α-smooth muscle actin(α-SMA)were detected by Western blotting.Results The expression level of miR-4645-5p in esophageal cancer tissues was signifi-cantly lower than that in adjacent tissues(P＜0.01).Compared with HET-1 A,the expression of miR-4645-5p was lower in esophageal cancer cell lines(P＜0.05).After overexpression of miR-4645-5p,the proliferation a-bility of KYSE-30 cells was significantly reduced(P＜0.05),the migration ability was significantly reduced(P＜0.01)and the invasion ability was significantly reduced(P＜0.01).miR-4645-5p targeted and negatively regulated the expression of MUC16 mRNA(P＜0.01).After overexpression of miR-4645-5p,the protein ex-pression levels of MUC16,ZEB-1 and α-SMA were all down-regulated,and the protein expression levels of ZO-1 and Claudin-1 were up-regulated.Conclusion miR-4645-5p regulates the malignant biological behavior of esophageal cancer KYSE-30 cells by targeting MUC16.
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Objective:To explore the role of DKK-1 andβ-catenin expressions in progression of proximal gastric cancer (PGC). Methods:The expression of DKK-1 andβ-catenin in 61 cases with PGC and para-neoplastic tissues and 20 cases with normal gastric mucosa was detected by immunohistochemistry. The related clinical significance in the cases was studied. Results:The positive expression rate of DKK-1 and the abnormal expression rate ofβ-catenin in the tissue sections of PGC were 34.4%(21/61) and 68.9%(42/61), respectively. The positive expression rate of DKK-1 and the abnormal expression rate ofβ-catenin in para-carcinoma tissues were 8.2%(5/61) and 6.6%(4/61) , respectively. The positive expression rate of DKK-1 and the abnormal expression rate ofβ-catenin in normal gastric mucosa were 15.0%(3/20) and 10.0%(2/20), respectively. The expression rate was significantly higher in PGC than that in the other tissues (P<0.05). The expression of DKK-1 was positively related to that ofβ-catenin in PGC (r=0.454, P<0.05), but not in the others. Conclusion:Higher expressions of DKK-1 and the abnormal expression ofβ-catenin are closely related to the occurrence of PGC.