PRKG1在前列腺癌中的表达及其机制

doi:10.3969/j.issn.2095-9400.2021.06.005

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摘要目的：研究cGMP依赖蛋白激酶1（PRKG1）在前列腺癌组织中的表达及其作用机制。方法：Western blot法检测前列腺癌的PRKG1表达。CRISPR/Cas9敲除22RV1细胞系的PRKG1基因，观察其对细胞增殖、迁移和侵袭能力的影响，并用Western blot法检测相关凋亡蛋白。结果：与正常前列腺组织组比，前列腺癌组织的PRKG1阳性率低（42.7% vs. 13.3%，P＜0.05），且不同肿瘤临床分期、Gleason评分阳性率差异无统计学意义（P＞0.05）。敲除PRKG1基因明显加强22RV1细胞系增殖、迁移和侵袭能力（P＜0.05）并导致Ezrin、MMP9、CDH-1、Bax水平显著降低（P＜0.05），CDH-2、Bcl-2水平升高（P＜0.05）。结论：PRKG1可能通过MMP9、CDH-2、Bax、Bcl-2和CDH-1蛋白抑制前列腺癌发生发展。

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关键词 ：前列腺癌, 环鸟苷酸依赖蛋白激酶1, 基因敲除

Abstract：Objective: To investigate the expression of PRKG1 in prostate cancer and its mechanism by knockout of prostate cancer cell line 22RV1. Methods: The expression of PRKG1 was detected by Western blot. The PRKG1 gene in prostate cancer cell line 22RV1 was knocked out by CRISPR/Cas9 and then its effect on proliferation, migration and invasion was observed and the related apoptotic protein was detected by Western blot. Results: The positive rate of PRKG1 in prostate cancer tissue was lower (42.7% vs. 13.3%, P<0.05), compared with normal prostate tissue. There was no significant difference between the two groups in clinical stage and Gleason score (P>0.05). Knockout of PRKG1 gene significantly enhanced the proliferation, migration and invasion of prostatic cacer cells (P<0.05). PRKG1 knockout significantly decreased the levels of Ezrin, MMP9, CDH-1 and Bax (P<0.05), but increased the levels of CDH-2 and Bcl-2 (P<0.05). Conclusion: PRKG1 can inhibit the development of prostate cancer through MMP9, CDH-2, Bax, Bcl-2 and CDH-1.

Key words： prostatic neoplasm cyclic GMP-dependent protein kinase type I gene knockout

收稿日期: 2021-01-03

基金资助:国家自然科学基金资助项目（81773092）。

作者简介: 饶大庞，副主任医师，Email：raodapang@tom.com。

链接本文:

https://xb.wmu.edu.cn/CN/10.3969/j.issn.2095-9400.2021.06.005 或 https://xb.wmu.edu.cn/CN/Y2021/V51/I6/454

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