长链非编码RNA PTENP1在膀胱癌发生发展中的分子机制

发布时间：2018-07-29 12:55

【摘要】：目的探讨长链非编码RNA PTENP1在膀胱癌发生发展中的分子机制。方法通过逆转录实时定量PCR(q RT-PCR)分别检测PTENP1,PTEN,miR-17在膀胱癌中的基础表达并关联分析。利用Western blot检测膀胱癌细胞系T24与5637中超表达PTENP1后PTEN的表达变化。通过荧光素酶报告试验验证miR-17对PTENP1及PTEN的靶向作用。最后通过在膀胱癌细胞系T24和5637中共表达miR-17和PTENP1,建立稳定共表达细胞系进行增殖和迁移实验,探索长链非编码RNA PTENP1在膀胱癌发生发展中的分子机制。结果 miR-17在膀胱癌中普遍呈现高表达趋势,PTENP1在膀胱癌中呈现普遍低表达趋势(P0.05)。与此同时miR-17和PTENP1的基础表达为负相关,PTENP1与PTEN的基础表达为正相关。WB实验发现于膀胱癌细胞系T24和5637中过表达PTENP1后可以在翻译水平增加PTEN的表达,荧光素酶报道实验验证了miR-17可同时靶向PTENP1及PTEN,在膀胱癌中miR-17具有促癌功能,同时在膀胱癌细胞中我们发现miR-17可以部分回复PTENP1的抑癌功能。结论长链非编码RNA PTENP1在膀胱癌中发挥抑癌功能的分子机制可能是PTENP1结合miR-17作为竞争性内源RNA竞争,从而降低miR-17对抑癌基因PTEN的表达抑制。
[Abstract]:Objective to investigate the molecular mechanism of long chain non-coding RNA PTENP1 in the carcinogenesis and development of bladder cancer. Methods the basic expression of PTENP1 and PTENN miR-17 in bladder cancer was detected by reverse transcriptase real time quantitative PCR (q RT-PCR. The changes of PTEN expression in bladder cancer cell lines T24 and 5637 after overexpression of PTENP1 were detected by Western blot. Luciferase report test was used to verify the targeting effect of miR-17 on PTENP1 and PTEN. Finally, miR-17 and PTENP1 were co-expressed in T24 and 5637 bladder cancer cell lines, and the stable co-expression cell lines were established to carry out proliferation and migration experiments to explore the molecular mechanism of long chain non-coding RNA PTENP1 in the development of bladder cancer. Results there was a high expression trend of miR-17 in bladder cancer and a general low expression trend of PTENP1 in bladder cancer (P0.05). At the same time, the basic expression of miR-17 and PTENP1 was negatively correlated with the basic expression of PTEN. WB assay showed that overexpression of PTENP1 in bladder cancer cell lines T24 and 5637 could increase the expression of PTEN at translation level. Luciferase reports have demonstrated that miR-17 can target both PTENP1 and PTEN in bladder cancer, and that miR-17 can promote cancer in bladder cancer. In bladder cancer cells, we found that miR-17 can partially restore the anti-tumor function of PTENP1. Conclusion the molecular mechanism of suppressor function of long chain noncoding RNA PTENP1 in bladder cancer may be that PTENP1 combined with miR-17 is a competitive endogenous RNA competition, thus reducing the inhibition of miR-17 on the expression of the tumor suppressor gene PTEN.
【作者单位】：华中科技大学同济医学院附属同济医院泌尿外科;澳门理工学院高等卫生学校;
【基金】：澳门理工学院科研项目(RP/ESS-03/2015)
【分类号】：R737.14

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