KIBRA promotes prostate cancer cell proliferation and motility

被引：28

作者：

Stauffer, Seth ^{[1
]}

Chen, Xingcheng ^{[1
]}

Zhang, Lin ^{[1
,2
]}

Chen, Yuanhong ^{[1
]}

Dong, Jixin ^{[1
]}

机构：

[1] Univ Nebraska Med Ctr, Fred & Pamela Buffett Canc Ctr, Eppley Inst Res Canc, Omaha, NE USA

[2] Shandong Univ, Qilu Hosp, Dept Radiat Oncol, Jinan 250100, Shandong, Peoples R China

来源：

FEBS JOURNAL | 2016年 / 283卷 / 10期

基金：

美国国家卫生研究院;

关键词：

AR signaling; KIBRA; motility; proliferation; prostate cancer; TUMOR-SUPPRESSOR; EPISODIC MEMORY; KINASE-ACTIVITY; GENE; EXPRESSION; ASSOCIATION; PROTEIN; HIPPO; PHOSPHORYLATION; GROWTH;

D O I：

10.1111/febs.13718

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

KIBRA is a regulator of the Hippo-yes-associated protein (YAP) pathway, which plays a critical role in tumorigenesis. In the present study, we show that KIBRA is a positive regulator in prostate cancer cell proliferation and motility. We found that KIBRA is transcriptionally upregulated in androgen-insensitive LNCaPC4-2 and LNCaP-C81 cells compared to parental androgen-sensitive LNCaP cells. Ectopic expression of KIBRA enhances cell proliferation, migration and invasion in both immortalized and cancerous prostate epithelial cells. Accordingly, knockdown of KIBRA reduces migration, invasion and anchorage-independent growth in LNCaP-C4-2/C81 cells. Moreover, KIBRA expression is induced by androgen signaling and KIBRA is partially required for androgen receptor signaling activation in prostate cancer cells. In line with these findings, we further show that KIBRA is overexpressed in human prostate tumors. Our studies uncover unexpected results and identify KIBRA as a tumor promoter in prostate cancer.

引用

页码：1800 / 1811

页数：12

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