LINC00680 Modulates Docetaxel Resistance in Breast Cancer via miR-320b/CDKL5 Axis

Abstract

BackgroundThe purpose of this study was to explore regulatory mechanism of the long non-coding RNA LINC00680 underlying the breast cancer chemoresistance via miR-205/CDKL5 axis. MethodsBioinformatics methods were applied to screen lncRNAs, miRNAs and mRNAs for construction of a competing endogenous RNA network. Dual-luciferase reporter assay were used to explore the relationship between LINC00680, miR-320b and CDKL5. CCK-8 assay and Transwell assay were utilized to evaluate the proliferation, migration and invasion in docetaxel-resistant cells.ResultsLINC00680 and CDKL5 protein levels were both up-regulated when induced by different concentration of docetaxel. LINC00680 knockdown decreased the expression level of drug resistance related genes (MDR1, MRP5, LRP1), proliferation, invasion of breast cancer cells. Bioinformatics prediction and dual-luciferase assay reveled that miR-320b both targeted the 3’-UTR of LINC00680 and CDKL5, suggesting that the modulation of LINC00680 on CDKL5 through sponging miR-320b. ConclusionsOverall, the results indicate the important role of LINC00680 in the docetaxel resistance through miR-320b/CDKL5 pathway, providing a novel therapy strategy for breast cancer drug resistance.