Linc00161 regulated the drug resistance of ovarian cancer by sponging microRNA-128 and modulating MAPK1

This study aimed to investigate the regulatory mechanism of linc00161/miR-128/MAPK1 axis on drug resistance of ovarian cancer. Methods: the differentially expressed lncRNAs were screened based on microarray analysis. The expression of linc00161, miR-128 and MAPK1 in ovarian cancer-resistant tissues and cells was tested qRT-PCR, whereas MAPK1 protein expression was examined via western blot in the ovarian cancer resistant cells. The targeted relationship between miR-128 and linc00161 as well as the relationship between miR-128 and MAPK1 were testified by Dual luciferase gene reporter assay. The influence of miR-128 and MAPK1 on the proliferation of ovarian cancer-resistant cells was demonstrated by CCK-8 and colony formation assay. The effect of linc00161 on ovarian cancer was demonstrated by xenograft tumor model in vivo. Results: Linc00161 was highly expressed in ovarian cancer-resistant tissues and SKOV3/DDP cells while the miR-128 displayed a lower expression. Overexpression of linc00161 increased the colony formation ratio in SKOV3 cells, whereas sh-linc00161 reduced colony formation ratio in SKOV3/DDP cells. MAPK1 was highly expressed in ovarian cancer-resistant tissues and cells and could be regulated by linc00161 and miR-128. The proliferation ability of SKOV3 cell was enhanced after transfected with miR-128 inhibitor, whereas that of SKOV3/DDP cells was attenuated by miR-128 mimics. In addition, the colony formation ratio of SKOV3 cells co-transfected with DDP + MAPK1 + sh-linc00161 decreased. The colony formation ratio of SKOV3/DDP cells also declined after transfected with DDP+ MAPK1. Linc00161 regulated the drug resistance of ovarian cancer via modulating microRNA-128/MAPK1. In vivo, sh-linc00161 inhibited the tumor growth.