Objective: To explore the molecular mechanism underlying the biological function of lncRNA PTENP1 in bladder cancer.
Methods: Expressions of PTENP1, PTEN and miR-17 were examined by quantitative reverse transcriptase PCR (qRT-PCR) in 12 bladder cancer tissues. The expression of PTEN was examined by Western blotting in bladder cancer cell lines T24 and 5637 overexpressing PTENP1. Luciferase reporter assay was performed to confirm the targeting of miR-17 to PTENP1 and PTEN. T24 and 5637 cell lines with stable overexpression of PTENP1 and mir-17 were used to investigate effect of PTNE and miR-17 on the function of PTENP1 in bladder cancer.
Results: The expression of miR-17 was up-regulated and PTENP1 and PTEN were down-regulated in bladder cancer tissues, where a positive correlation was found between PTENP1 and PTEN expressions and a negative correlation between PTENP1 and miR-17 (P<0.05). Overexpression of PTENP1 in bladder cancer cell lines T24 and 5637 obviously enhanced the expression of PTEN protein. miR-17 was found to target both PTENP1 and PTEN and promote the growth of bladder cancer. miR-17 could partially restore the tumor-suppressing activity of PTENP1 in bladder cancer.
Conclusion: By binding with miR-17, lncRNA PTENP1 functions as a PTEN competing endogenous RNA (ceRNA) to suppress the progression of bladder cancer.
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（qRT-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。