PTPRJ通过Src/PI3K/Akt信号通路促进前列腺癌细胞的黏附、迁移和侵袭  

PTPRJ promotes the adhesion,migration and invasion of prostate cancer cells through Src/PI3K/Akt signaling pathway

作　　者：朱宝安[1] 郑建新[2] 张印坡[3] ZHU Baoan;ZHENG Jianxin;ZHANG Yinpo(Department of Biochemistry,Luohe Medical College,Henan Luohe 462002,China;The Second Hospital to Luohe Medical College,Henan Luohe 462002,China;Pathological Examination Center,Luohe Medical College,Henan Luohe 462002,China)

机构地区：[1]漯河医学高等专科学校生物化学教研室,河南漯河462002 [2]漯河医学高等专科学校第二附属医院,河南漯河462002 [3]漯河医学高等专科学校病理检测中心,河南漯河462002

出　　处：《现代肿瘤医学》2023年第13期2437-2442,共6页Journal of Modern Oncology

基　　金：河南省高等职业学校青年骨干教师培养计划(编号:2019GZGG091)。

摘　　要：目的:探究PTPRJ基因表达对前列腺癌DU145细胞黏附、迁移和侵袭的影响以及可能的调控机制。方法:实时荧光定量PCR、Western blot检测PTPRJ在前列腺肿瘤组织和细胞系中的表达;用携带PTPRJ特异shRNA的重组慢病毒(LV-shPTPRJ)感染沉默PTPRJ表达;MTT检测细胞黏附力,Transwell检测细胞迁移和侵袭;实时荧光定量PCR、Western blot检测信号通路分子mRNA和蛋白表达。结果:与正常前列腺组织和细胞相比,PTPRJ在前列腺肿瘤组织和PC-3、DU145细胞系中表达升高(P<0.05);与对照组相比,沉默PTPRJ后前列腺癌DU145细胞黏附、迁移和侵袭能力显著下降(P<0.01)、信号通路蛋白p^(Y418)Src、p-PI3K和p-Akt表达水平均显著降低(P<0.05);SC79激活PI3K/Akt可逆转PTPRJ下调对DU145细胞黏附和侵袭的影响;沉默PTPRJ下调裸鼠瘤体组织中p^(Y418)Src、p-PI3K和p-Akt表达(P<0.05)。结论:PTPRJ可能通过激活Src/PI3K/Akt信号通路来促进DU145细胞的黏附、迁移和侵袭,预示PTPRJ可能成为前列腺癌治疗的潜在靶点。Objective:To investigate the effects of PTPRJ gene expression on the adhesion,migration and invasion of DU145 cells of prostate cancer and the possible regulatory mechanism.Methods:Real-time quantitative PCR and Western blot were used to detect the expression of PTPRJ in prostate tumor tissues and cell lines.PTPRJ expression was silenced by infecting cells with recombinant lentivirus(LV-shPTPRJ)carrying PTPRJ-specific shRNA.Cell adhesion was detected by MTT,cell migration and invasion were detected by Transwell.Real-time quantitative PCR and Western blot were used to detect the mRNA and protein expression of signaling pathway molecules.Results:Compared with normal prostate tissues and cells,PTPRJ expression was increased in prostate tumor tissues and PC-3 and DU145 cell lines(P<0.05).Compared with the control group,the adhesion,migration and invasion ability of DU145 cells were significantly decreased after PTPRJ silencing(P<0.01),and the expression levels of signaling pathway proteins p^(Y418) Src,p-PI3K and p-Akt were significantly decreased(P<0.05).Activation of PI3K/Akt by SC79 reversed the effect of PTPRJ downregulation on DU145 cell adhesion and invasion.Silencing PTPRJ down-regulated the expression of p^(Y418) Src,p-PI3K and p-Akt in the tumor tissue of nude mice(P<0.05).Conclusion:PTPRJ may promote the adhesion,migration and invasion of DU145 cells by activating the Src/PI3K/Akt signaling pathway,indicating that PTPRJ may be a potential target for prostate cancer treatment.

关 键 词：受体型酪氨酸磷酸酶J 前列腺癌细胞DU145 Src/PI3K/Akt信号通路 

分 类 号：R737.25[医药卫生—肿瘤]