基础医学与临床 ›› 2017, Vol. 37 ›› Issue (12): 1706-1711.

• 研究论文 • 上一篇    下一篇

miR-29c促进前列腺癌PC3细胞凋亡

刘南京1,李婷1,赵燕1,郝燕妮1,吴小候2,罗春丽3   

  1. 1. 重庆医科大学
    2. 重庆医科大学附属第一医院
    3. 重庆医科大学检验医学院
  • 收稿日期:2016-12-01 修回日期:2017-01-18 出版日期:2017-12-05 发布日期:2017-11-29
  • 通讯作者: 罗春丽 E-mail:luochunli79@126.com
  • 基金资助:
    hepaCAM粘附分子丢失诱导膀胱癌的侵袭转移机制

miR-29c promotes apoptosis in prostate cancer cell line PC3

  • Received:2016-12-01 Revised:2017-01-18 Online:2017-12-05 Published:2017-11-29
  • Contact: LUO Chun-li E-mail:luochunli79@126.com

摘要: 目的 研究miR-29c对前列腺癌PC3细胞凋亡的影响及其机制。方法 以人正常前列腺上皮细胞(RWPE-1)为对照,检测前列腺癌PC3细胞中miR-29c、血管内皮生长因子(VEGF)及血管内皮生长因子受体2(VEGFR2)的表达;IF检测p-VEGFR2在细胞中的定位。miR-29c过表达腺病毒转染PC3,RT-PCR检测miR-29c及VEGF的表达;Western blot检测VEGF、t-VEGFR2、p-VEGFR2、BAX和Bcl-2的表达;hoechst 33258 染色法检测PC3细胞凋亡;流式细胞术(FCM)检测PC3细胞早期凋亡率。结果 与RWPE-1相比,PC3细胞miR-29c表达降低,VEGF及VEGFR2表达升高(p<0.001);与对照组相比,miR-29c过表达组VEGF、p-VEGFR2及Bcl-2的表达显著降低(p<0.001),BAX的表达显著升高(p<0.001),细胞凋亡与早期凋亡率显著增加(p<0.001)。结论 重新表达miR-29c可以显著抑制VEGF/VEGFR2信号通路并促进PC3细胞凋亡。

关键词: 前列腺癌, miR-29c, 血管内皮生长因子, 血管内皮生长因子受体

Abstract: Objective To study the effect of miR-29c on the apoptosis of prostate cancer cell line PC3. Methods The expression of miR-29c, VEGF and VEGFR2 in RWPE-1 and PC3 were detected to verify the different between normal and Cancer cell. The location of p-VEGFR2 was measured by immunofluorescence (IF). After PC3 cell were transfected by miR-29c overexpression adenovirus , the expression level of miR-29c, VEGF, t-VEGFR2, p-VEGFR2, BAX and Bcl-2 were measured by RT-PCR and Western blot , the cell apoptosis rate was detected by the kits of hoechst 33258 and FCM. Results The expression level of miR-29c was lower and VEGF, VEGFR2 was higher in PC3 cell compared with that in RWPE-1(p<0.001). The expression level of miR-29c and BAX were higher and VEGF, P-VEGFR2 and Bcl-2 were lower in Ad-miR-29c group compared with that in control group(p<0.001). Higher apoptosis rate was detected in Ad-miR-29c group compared with control group(p<0.001). Conclusions miR-29c can promotes apoptosis in prostate cancer cell PC3 by inhibiting VEGF/VEGFR2 signaling.

Key words: prostate cancer, miR-29c, VEGF, VEGFR2

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