GLI1, a crucial mediator of sonic hedgehog signaling in prostate cancer, functions as a negative modulator for androgen receptor

被引：41

作者：

Chen, Guangchun ^{[1
]}

Goto, Yutaka ^{[1
]}

Sakamoto, Ryuichi ^{[1
]}

Tanaka, Kimitaka ^{[1
]}

Matsubara, Eri ^{[1
]}

Nakamura, Masafumi ^{[2
]}

Zheng, Hong ^{[3
]}

Lu, Jian ^{[4
]}

Takayanagi, Ryoichi ^{[1
]}

Nomura, Masatoshi ^{[1
]}

机构：

[1] Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioregulatory Sci, Fukuoka 8128582, Japan

[2] Kyushu Univ, Grad Sch Med Sci, Dept Canc Therapy & Res, Fukuoka 8128582, Japan

[3] Second Mil Med Univ, Sch Pharm, Shanghai 200433, Peoples R China

[4] Second Mil Med Univ, Dept Pathophysiol, Shanghai 200433, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2011年 / 404卷 / 03期

关键词：

Androgen receptor; Sonic hedgehog; GLI1; Prostate cancer; GENE-EXPRESSION; INHIBITION; PATHWAY; DOMAIN; TRANSCRIPTION; ACTIVATION; CELLS; TARGETS; BINDING;

D O I：

10.1016/j.bbrc.2010.12.065

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：

Sonic hedgehog (SHH) signaling, acting in a combinatorial manner with androgen signaling, is essential for prostate patterning and development. Recently, elevated activation of SHH signaling has been shown to play important roles in proliferation, progression and metastasis of prostate cancer. In this report, we demonstrate for the first time, that GLI1, which has been shown to play a central role in SHH signaling in prostate cancer, can act as a co-repressor to substantially block androgen receptor (AR)-mediated trans-activation, at least in part, by directly interacting with AR. Our observations suggest that the SHH-GLI pathway might be one of determinants governing the transition of prostate cancer from an androgen-dependent to an androgen-independent state by compensating, or even superseding androgen signaling. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：809 / 815

页数：7

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