Prostate specific membrane antigen knockdown impairs the tumorigenicity of LNCaP prostate cancer cells by inhibiting the phosphatidylinositol 3-kinase/Akt signaling pathway

作     者：Guo Zhenghui Lai Yiming Du Tao Zhang Yiming Chen Jieqing Bi Liangkuan Lin Tianxin Liu Hao Wang Wei Xu Kewei Jiang Chun Han Jinli Zhang Caixia Dong Wen Huang Jian Huang Hai 

作者机构：Department of Urology Sun Yat-sen Memorial Hospital Sun Yat-sen University Guangzhou Guangdong 510120 China 

出 版 物：《Chinese Medical Journal》 (中华医学杂志（英文版）)

年 卷 期：2014年第127卷第5期

页      面：929-936页

核心收录：

学科分类：0710[理学-生物学] 081702[工学-化学工艺] 07[理学] 08[工学] 0817[工学-化学工程与技术] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种] 

基　　金：This study was supported by grants from the grants from the National Natural Science Foundation of China the National Natural Science Foundation of China for the Young Scientists Grant the Guangdong Province Natural Science Foundation 

主　　题：prostate cancer LNCaP cells prostate-specific membrane antigen RNA interference PI3K/Akt pathway tumorigenicity 

摘      要：Background Prostate specific membrane antigen （PSMA） can facilitate the growth,migration,and invasion of the LNCaP prostate cancer cell lines,but the underlying molecular mechanisms have not yet been clearly ***,we investigated whether PSMA serves as a novel regulator of the phosphatidylinositol 3-kinase （PI3K）/Akt signaling by employing PSMA knockdown model and PI3K pharmacological inhibitor （LY294002） in LNCaP prostate cancer *** PSMA knockdown had been stably established by transfecting with lentivirus-mediated siRNA in our previous ***,LNCaP cells were divided into interference,non-interference,and blank *** first testified the efficacy of PSMA knockdown in our LNCaP cell ***,we compared the expression of PSMA and total/activated Akt by Westem blotting in the above three groups with or without LY294002 ***,immunocytochemistry was performed to confirm the changes of activated Akt （p-Akt,Ser473） in ***,cell proliferation,migration,and cell cycle were measured by CCK-8 assay,Transwell analysis,and Flow cytometry *** After PSMA knockdown,the level of p-Akt （Ser473） but not of total-Akt （Akt1/2） was significantly decreased when compared with the non-interference and blank ***,LY294002 administration significantly reduced the expression of p-Akt （Ser473） in all the three *** results of immunocytochemistry further confirmed that PSMA knockdown or LY294002 treatment was associated with p-Akt （Ser473） *** of cell proliferation,migration,and survival were also observed upon PSMA knockdown and LY294002 *** Taken together,our results reveal that PI3K/Akt signaling pathway inhibition may serve as a novel molecular mechanism in LNCaP prostate cancer cells of PSMA knockdown and suggest that Akt （Ser473） may play a critical role as a downstream signaling target effector of PSMA in this cellular model.