Epigenetic silencing of miR-130b in ovarian cancer promotes the development of multidrug resistance by targeting colony-stimulating factor 1

摘要: Abstract Objective The purpose of this study was to investigate the role miR-130b in development multidrug-resistant ovarian cancer. Methods expression assessed tissues and cell lines by qRT-PCR. In vitro, level manipulated transfection with mimics or inhibitors. Methylation evaluated quantitative methylation-specific PCR (qMSP). CSF-1 cells determined qRT-PCR, immunohistochemistry ELISA, respectively. regulated detected using Dual Luciferase Reporter system. Results Down-regulation cancer associated FIGO III–IV clinical stages poorer histological differentiation. MiR-130b downregulated multidrug resistant cells. Restoration could sensitize these anticancer drugs. hypermethylation found as well drug methylation negatively correlated its expression. Demethylation 5-aza-CdR led reactivation concomitant increase sensibility cisplatin taxol. lines. assay validated is a direct target miR-130b. Knock-down sensitized drugs partially attenuate resistance inducing effect Conclusions Downregulation promotes targeting 3′-UTR CSF-1, silencing may be mediated DNA methylation.