Effects of high expression of miR 19a in hepatocellular carcinoma tissues on the epithelial mesenchymal transition in HepG2 cells

WANG Liping; SUN Shiping; HUA Zhengxiang

doi:10.3969/j.issn.1002-7386.2018.10.002

Abstract：Objective To investigate the expression of microRNA (microRNA,miRNA,miR) 19a in hepatocellular carcinoma tissues and the effects of miR-19a on epithelial-mesenchymal transition (EMT) in hepatocellular cell line-HepG2.Methods Quantificational real time polymerase chainreaction (qRT PCR) was used to measure the expression levels of miR-19a in hepatocellular carcinoma tissues and corresponding para-carcinoma tissues in 25 patients with hepatic carcinoma.The MiR 19a mimic or negative control of miR 19a (miR NC) were transfected into HepG2 with low expressions of miR 19a.The expression levels of miR 19a in HepG2 cells were detected by qRT PCR,moreover MTT and Transwell small chamber method were used to measure the abilities of proliferation and migration of the cells.In addition,the expression levels of Ecad,N-cad,Vimentin mRNA and proteins were detected by qRT PCR and Western Blot after miR 19a mimic was transfected into HepG2 cells.Results The expression levels of miR-19a in hepatocellular carcinoma tissues were significantly higher than those in paracancerous tissues (P ＜ 0.01).After miR-19a-mimic was transfected into HepG2 cells,the expression levels of miR-19a were significantly higher than those in negative control group (P ＜ 0.01),and the proliferation and migration abilities of cells were significantly higher than those in negative control group (P ＜ 0.01).Moreover the expression levels of E-cad mRNA and proteins were significantly lower than those in negative control group (P ＜ 0.01),however the expression levels of N cad,Vimentin mRNA and proteins in HepG2 cells were significantly higher than those in negative control group (P ＜ 0.01).Conclusion The high expression levels of MiR 19a exist in hepatocellular carcinoma tissues,which can promote the proliferation and migration ablities of HepG2 cells and induce the EMT of HepG2 cells.