Fetuin B overexpression suppresses proliferation, migration, and invasion in prostate cancer by inhibiting the PI3K/AKT signaling pathway

被引:19
作者
Zhan, Kai [1 ,2 ]
Liu, Rui [3 ]
Tong, Hang [1 ,2 ]
Gao, Shun [1 ,2 ]
Yang, Guang [1 ,2 ]
Hossain, Arman [1 ]
Li, Tinghao [1 ,2 ]
He, Weiyang [1 ]
机构
[1] Chongqing Med Univ, Affiliated Hosp 1, Dept Urol, 1 Youyi Rd, Chongqing 400016, Peoples R China
[2] Chongqing Med Univ, Affiliated Hosp 1, Cent Lab, Chongqing 400016, Peoples R China
[3] Chongqing Med Univ, Affiliated Hosp 2, Dept Oncol, Chongqing 400010, Peoples R China
基金
中国国家自然科学基金;
关键词
Fetuin B (FETUB); Prostate cancer; PI3K/AKT; Epithelial-mesenchymal transition (EMT); CARCINOMA-CELL-LINE; PROTEIN; PROGRESSION; EXPRESSION; STEATOSIS; APOPTOSIS; FAMILY; MEMBER; LIVER; EMT;
D O I
10.1016/j.biopha.2020.110689
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Fetuin B (FETUB) is a glycoprotein that is a member of the cysteine protease inhibitor family, and it is associated with cancer. However, the role of FETUB in prostate carcinogenesis is unknown. In this study, we overexpressed FETUB in prostate cancer cells by using lentivirus and then studied the impacts on cell apoptosis, migration and invasion. We found that apoptosis was increased and the migration and invasion of prostate cancer cells were significantly inhibited after overexpression. Then, we performed experiments in vivo and found that there were fewer tumors in the overexpression groups than in the control groups. In addition, we demonstrated that overexpression of FETUB inactivates the PI3K/AKT signaling pathway. Rescue assays revealed that intervention of 740Y-P reversed the anti-tumor effect of FETUB on prostate cancer cells. Taken together, our results revealed that FETUB may act as a novel regulator to promote apoptosis and inhibit the migration and invasion of prostate cancer cells and that FETUB is related to the inactivation of the PI3K/AKT signaling pathway.
引用
收藏
页数:13
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