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.
Significance
We demonstrated that overexpression of Linc00518 contributed to the paclitaxel resistance in prostate cancer via sequestering miR-216b-5p.