Effects of interfering lncRNA-C2orf48 expression on proliferation,migration and invasion of HepG2 cells and their possible mechanism
Objective To observe the effects of interfering the expression of long non-coding RNA C2orf48(lncRNA-C2orf48)on proliferation,migration and invasion of human hepatoma cell line HepG2,and to explore the possible mecha-nism.Methods Human normal hepatocellular cell line LO2 and hepatocellular carcinoma cell lines HepG2 and Huh-7 were cultured in vitro.The relative expression of lncRNA-C2orf48 was detected by real-time fluorescence quantitative PCR(RT-PCR).HepG2 cells with a good growth state and a confluent rate of 90%were selected and divided into three groups.Cells in the si-C2orf48 group were transfected with lncRNA-C2orf48 silence sequence(si-C2orf48),si-NC group with nega-tive control sequence(si-NC),and cells in the Blank group were not treated.The cell proliferation rate was measured by CCK-8 assay,and cell migration and membrane penetration were measured by Transwell assay,respectively.The relative expression levels of lncRNA-C2orf48,microRNA 519d-3p(miR-519d-3p)and ribonucleotide reductase M2(RRM2)were detected by RT-PCR.Results Compared with L02 cells,the relative expression levels of lncRNA-C2orf48 in both HepG2 and HuH-7 cells increased(both P<0.05),and the increase was more obvious in HepG2 cells.HepG2 cells were selected as the follow-up experiment subjects.Compared with the Blank group and si-NC group,the cell proliferation rate,the number of migration cells and the number of transmembrane cells decreased,the relative expression levels of lncRNA-C2orf48 and RRM2 RNA decreased,and the relative expression levels of miR-519d-3p RNA increased in the si-C2orf48 group(all P<0.05).Conclusion LncRNA C2orf48 is overexpressed in HepG2 cells,and interfering lncRNA-C2orf48 can significantly inhibit the proliferation,migration and invasion of HepG2 cells,and the possible mechanism may be that the interfering LncRNA C2orf48 promotes the overexpression of miR-519d-3p,resulting in the decrease of RRM2 expression.