蛋白质精氨酸甲基转移酶6调控前列腺癌发生的分子机制  

Molecular Mechanism of Protein Arginine Methyl transferase 6 Regulated Prostate Cancer

作　　者：徐莹[1] 阎英[1] 柳云恩[2] 

机构地区：[1]沈阳军区总医院放射治疗科,沈阳110840 [2]沈阳军区总医院急诊医学部全军重症战创伤救治中心实验室,沈阳110840

出　　处：《成都医学院学报》2015年第4期420-427,共8页Journal of Chengdu Medical College

基　　金：辽宁省科技攻关课题(No:2012225008)

摘　　要：目的探讨蛋白质精氨酸甲基转移酶6(PRMT6)调控前列腺癌发生的分子机制。方法通过免疫组织化学、Western blot、Real Time PCR、转染、克隆实验、流式细胞技术和Transwell实验研究PRMT6对前列腺癌细胞增殖、细胞周期及迁移的影响。结果研究发现,PRMT6在前列腺癌组织及前列腺癌细胞系中呈高表达状态,PRMT6表达改变与促癌基因PSA和KLK2成正相关,证实PRMT6通过调控AR下游靶基因促进前列腺癌发生。此外,PRMT6促进前列腺癌细胞22Rv1和LNCaP的细胞周期进程,促进细胞增殖及迁移。结论 PRMT6通过调控AR下游靶基因促进前列腺癌细胞的增殖及迁移,从而促进前列腺癌的发生发展。Objective To investigate the molecular mechanism of PRMT6（protein arginine methyl transferase 6） in the regulation of prostate cancer. Methods The effects of PRMT6 on the proliferation, cell cycle and migration of prostate cancer cells were studied by immunohistochemistry, Real-time PCR, Western blot, flow cytometry and transwell assay. Results PRMT6 was highly expressed in prostate cancer tissues and prostate cancer cell lines, and the expression of PRMT6 was positively correlated with KLK2 and PSA, which was confirmed by AR regulating the PRMT6 downstream target gene to promote prostate cancer. Conclusion PRMT6 can promote the proliferation and migration of prostate cancer cells through regulating the AR downstream target gene, and thus promote the development of prostate cancer.

关 键 词：前列腺癌 蛋白质精氨酸甲基转移酶6 凋亡 分子机制 

分 类 号：Q555[生物学—生物化学]