He Junhui, Sun Mingchong, Geng Huaizhen, Tian Sujian
Department of Urology Surgery, Heze Municipal Hospital, Heze, 274000, China.
Biol Cell. 2019 Feb;111(2):39-50. doi: 10.1111/boc.201800054. Epub 2018 Dec 7.
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.
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.
We demonstrated that overexpression of Linc00518 contributed to the paclitaxel resistance in prostate cancer via sequestering miR-216b-5p.
为了表征Linc00518在前列腺癌中的表达，并阐明其在紫杉醇耐药性中潜在的机制参与，通过实时PCR测定Linc00518和miR-216b-5p的相对表达。用荧光素酶报告基因测定法研究miR-216b-5p对Linc00518或GATA6的调控作用。通过蛋白质印迹法分析内源性GATA6蛋白。用MTT法测定细胞活力，并通过细胞计数计算紫杉醇的IC50。
Linc00518在体内和体外的前列腺肿瘤中均高表达。高水平的Linc00518转录本与紫杉醇耐药性相关。Linc00518通过海绵机制竞争性抑制miR-216b-5p。Linc00518缺陷损害了获得性耐药细胞系中的紫杉醇耐药性。
我们证明Linc00518的过表达通过隔离miR-216b-5p导致前列腺癌中的紫杉醇耐药性。
