miR-200c inhibits proliferation in bladder cancer cells through down-regulation of KRAS

李建昌; 苏泽轩; 石利平; 陈合格; 柳建军; 刘磊

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miR-200c inhibits proliferation in bladder cancer cells through down-regulation of KRAS

更新时间：2026-01-09

- miR-200c inhibits proliferation in bladder cancer cells through down-regulation of KRAS
- Journal of Army Medical University Vol. 37, Issue 21, Pages: 2142-2146(2015)
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  CLC： R394.3;R730.23;R737.14
- Published：2015
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李建昌,苏泽轩,石利平,陈合格,柳建军,刘磊.miR-200c下调KRAS基因表达抑制膀胱癌细胞体外增殖能力[J].陆军军医大学学报(原第三军医大学学报),2015,37(21):2142-2146.

　Li Jianchang,Su Zexuan,Shi Liping,Chen Hege,Liu Jianjun,Liu Lei.miR-200c inhibits proliferation in bladder cancer cells through down-regulation of KRAS[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(21):2142-2146.
李建昌,苏泽轩,石利平,陈合格,柳建军,刘磊.miR-200c下调KRAS基因表达抑制膀胱癌细胞体外增殖能力[J].陆军军医大学学报(原第三军医大学学报),2015,37(21):2142-2146. DOI：

　Li Jianchang,Su Zexuan,Shi Liping,Chen Hege,Liu Jianjun,Liu Lei.miR-200c inhibits proliferation in bladder cancer cells through down-regulation of KRAS[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(21):2142-2146. DOI：

摘要

目的探讨miR-200c对膀胱癌细胞体外增殖能力的作用及机制。方法慢病毒感染法建立稳定过表达和稳定低表达miR-200c膀胱癌细胞，分为对照组、稳定过表达miR-200c组（miR-200c组）、稳定低表达miR-200c组（miR-200c-inhibit组），实时定量qRT-PCR和Western blot检测不同实验组膀胱癌细胞中miR-200c、KRAS的表达量，克隆试验检测不同组膀胱癌细胞系的增殖能力。结果 CCK-8试验显示对照组T24和UM-UC-3与miR-200c组分别为0.833 3±0.062 1、0.650 3±0.088 7和0.939 0±0.018 1、0.806 0±0.021 6，2组间差异有统计学意义（T24，P0.05；UM-UC-3，P0.01）。稳定过表达miR-200c后，膀胱癌细胞系内KRAS蛋白的表达降低(P0.05)。结论 miR-200c在体外通过下调KRAS基因降低膀胱癌细胞的增殖能力。

Abstract

Objective To determine the role and underlying mechanism of miR-200c in the proliferation of bladder cancer. Methods After lentiviruses were used to stably over-express and antagonize miR-200c in bladder cancer 5637

TCC-SUP and UM-UC-3 cells

RT-qPCR and Western blotting were intended to detect the expression changes of miR-200c and KRAS. Dual luciferase reporting system was used to verify whether miR-200c regulated the 3′UTR of KRAS as target. Colony formation assay was applied to analyze the change of colony formation abilities of bladder cancer cells in different groups. Results CCK-8 assay that cell viability was 0.833 3±0.062 1 and 0.650 3±0.088 7 in the controlled and miR-200c T24 cells (P0.05)

and 0.939 0±0.018 1 and 0.806 0±0.021 6 in the controlled and miR-200c UM-UC-3 cells (P0.01). Stably over-expression of miR-200c resulted in significant decrease in protein expression of KRAS (P0.05). Conclusion miR-200c suppresses the proliferation of bladder cancer cells by down-regulating the expression of KRAS protein

which indicates that KRAS plays a vital role in the incidence and progression of bladder cancer.

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