Abstract
BackgroundEpithelial ovarian cancer (EOC) has a high mortality rate and is a common malignant tumor of women, seriously impairing health. Chemoresistance is one of the major causes of poor prognosis. Therefore, analyzing the molecular mechanism of paclitaxel resistance has great significance.Material/MethodsWe analyzed aberrantly expressed lncRNAs in chemoresistant EOC cells by microarray and confirmed LINC01118 expression by real-time PCR. The paclitaxel sensitivity alternation was analyzed by MTS, flow cytometry, and Transwell assay, while wound healing assays were performed to assess apoptosis, migration, and invasion in vitro. The interaction between LINC01118 and miR-134 was confirmed by luciferase assay.ResultsLINC01118 was highly expressed in EOC tissues and chemoresistant cells. Biological function experiments showed LINC01118 could facilitate paclitaxel resistance and promote migration and invasion while inhibiting apoptosis of EOC cells. Moreover, LINC01118 targets miR-134 and then affects ABCC1 expression.ConclusionsLINC01118 acted as an oncogene and modulated EOC paclitaxel sensitivity by regulating miR-134/ABCC1.
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