慢病毒短发夹RNA介导的多形性腺瘤基因样蛋白2沉默对肝癌细胞MHCC97-L增殖、迁移及侵袭的影响

目的 探讨慢病毒短发夹RNA(shRNA)介导的多形性腺瘤基因样蛋白2(PLAGL2)沉默对肝癌细胞恶性行为的影响及其机制.方法 Real-time PCR与Western blotting分别检测肝癌组织及癌旁组织中PLAGL2的表达水平;体外培养肝癌细胞MHCC97-L,构建慢病毒载体质粒PLAGL2-shRNA与...

Effect of short hairpin RNA lentivirus-mediated silencing of pleomorphic adenoma gene like-2 on proliferation,migration and invasion of hepatocellular carcinoma cells

Objective To investigate the effect of short hairpin RNA(shRNA)-mediated pleomorphic adenoma gene like-2(PALAG2)silencing on the malignant behavior of hepatocellular carcinoma cells and its mechanism.Methods Real-time PCR and Western blotting were used to detect the expression level of PLAGL2 in liver cancer tissues and adjacent tissues.Hepatoma cells MHCC97-L were cultured in vitro,the lentiviral vector plasmid PLAGL2-shRNA and control NC-shRNA were constructed,transfected into MHCC97-L cells,and stable transfected strains were selected with puromycin.CCK-8 and Transwell chamber assay detected the proliferation activity and the number of migration and invasion of MHCC97-L cells after silencing PLAGL2.Western blotting was used to detect the expression of p-PI3 K and p-Akt proteins.The PI3 K/Akt signaling pathway activator was used to treat MHCC97-L cells to detect cell proliferation,migration and invasion.Results The expression of PLAGL2 was significantly increased in liver cancer tissue(P<0.05).Transfection of 9 strains of MHCC97-L cells with PLAGL2-shRNA could significantly reduce the expression level of PLAGL2,and the ability of proliferation,migration,and invasion of MHCC97-L cells was also weakened(P<0.05),and the expression levels of p-PI3 K,and p-Akt were inhibited(P<0.05),PI3 K/Akt activator could obviously reverse the above phenomenon.Conclusion shRNA lentiviral vector pathway can effectively silence the expression of PLAGL2 gene in hepatocarcinoma cells.Silencing of PLAGL2 can significantly inhibit the malignant behavior of proliferation,migration and invasion of hepatocarcinoma cells,and its mechanism may be related to the inhibition of PI3 K/Akt signaling pathway activation.