Rap2B promotes cell proliferation, migration and invasion in prostate cancer

被引:17
|
作者
Di, Jiehui [1 ]
Cao, Huan [1 ]
Tang, Juangjuan [1 ,4 ]
Lu, Zheng [1 ]
Gao, Keyu [1 ]
Zhu, Zhesi [1 ]
Zheng, Junnian [1 ,2 ,3 ]
机构
[1] Xuzhou Med Coll, Inst Canc, Xuzhou 221002, Jiangsu, Peoples R China
[2] Xuzhou Med Coll, Inst Canc, Jiangsu Ctr Collaborat & Innovat Canc Biotherapy, Xuzhou 221002, Jiangsu, Peoples R China
[3] Xuzhou Med Coll, Affiliated Hosp, Ctr Clin Oncol, Xuzhou 221002, Jiangsu, Peoples R China
[4] Xuzhou Med Coll, Affiliated Hosp, Dept Oncol, Xuzhou 221002, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Rap2B; FAK; Prostate cancer; Migration; FOCAL ADHESION KINASE; DIFFERENTIALLY EXPRESSED GENES; LUNG-CANCER; BREAST-CANCER; P53; TARGET; IDENTIFICATION; METASTASIS; CARCINOMA; PATHWAYS; PROTEINS;
D O I
10.1007/s12032-016-0771-7
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Rap2B, a member of the Ras family of small GTP-binding proteins, reportedly presents a high level of expression in various human tumors and plays a significant role in the development of tumor. However, the function of Rap2B in prostate cancer (PCa) remains unclear. We elucidated the stimulative role of Rap2B in PCa cell proliferation, migration and invasion by means of the CCK-8 cell proliferation assay, cell cycle analysis and transwell migration assay. Western blot analysis uncovered that elevated Rap2B leads to increased phosphorylation levels of FAK, suggesting that FAK-dependent pathway might be responsible for the effect of Rap2B on PCa cells migration and invasion. Inversely, FAK-specific inhibitor (PF-573228) can abort Rap2B-induced FAK phosphorylation. In vivo experiment confirmed that Rap2B positively regulated PCa growth and metastasis, as well as the expression of phosphorylated FAK. Collectively, these findings shed light on Rap2B as a potential therapeutic target for PCa.
引用
收藏
页数:10
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