BACKGROUND INFORMATION: To characterise Linc00518 expression in prostate cancer and elucidate the potential mechanistic involvement in paclitaxel resistance, the relative expression of Linc00518 and miR-216b-5p was determined by real-time PCR. The regulatory effect of miR-216b-5p on either Linc00518 or GATA6 was interrogated with luciferase reporter assay. The endogenous GATA6 protein was analysed by Western blotting. The cell viability was measured by MTT assay and IC50 of paclitaxel was calculated through cell counting. RESULTS: Linc00518 was highly expressed in prostate tumour both in vivo and in vitro. High level of Linc00518 transcripts associated with paclitaxel resistance. Linc00518 competitively inhibited miR-216b-5p through sponging mechanism. Linc00518 deficiency compromised the paclitaxel resistance in the acquired resistance cell lines. CONCLUSIONS AND SIGNIFICANCE: We demonstrated that overexpression of Linc00518 contributed to the paclitaxel resistance in prostate cancer via sequestering miR-216b-5p.
BACKGROUND INFORMATION: To characterise Linc00518 expression in prostate cancer and elucidate the potential mechanistic involvement in paclitaxel resistance, the relative expression of Linc00518 and miR-216b-5p was determined by real-time PCR. The regulatory effect of miR-216b-5p on either Linc00518 or GATA6 was interrogated with luciferase reporter assay. The endogenous GATA6 protein was analysed by Western blotting. The cell viability was measured by MTT assay and IC50 of paclitaxel was calculated through cell counting. RESULTS:Linc00518 was highly expressed in prostate tumour both in vivo and in vitro. High level of Linc00518 transcripts associated with paclitaxel resistance. Linc00518 competitively inhibited miR-216b-5p through sponging mechanism. Linc00518 deficiency compromised the paclitaxel resistance in the acquired resistance cell lines. CONCLUSIONS AND SIGNIFICANCE: We demonstrated that overexpression of Linc00518 contributed to the paclitaxel resistance in prostate cancer via sequestering miR-216b-5p.