TY - JOUR
T1 - GLI1, a crucial mediator of sonic hedgehog signaling in prostate cancer, functions as a negative modulator for androgen receptor
AU - Chen, Guangchun
AU - Goto, Yutaka
AU - Sakamoto, Ryuichi
AU - Tanaka, Kimitaka
AU - Matsubara, Eri
AU - Nakamura, Masafumi
AU - Zheng, Hong
AU - Lu, Jian
AU - Takayanagi, Ryoichi
AU - Nomura, Masatoshi
N1 - Funding Information:
We thank Dr. Shigeaki Kato, Hiroshi Sasaki, Jer-Tsong Hsieh, and Pierre Chambon for kindly donating the plasmids. This work was supported in part by a grant-in-aid for Scientific Research from the Ministry of Education, Science, Sports and Culture, Japan.
PY - 2011/1/21
Y1 - 2011/1/21
N2 - 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 transactivation, 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.
AB - 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 transactivation, 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.
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U2 - 10.1016/j.bbrc.2010.12.065
DO - 10.1016/j.bbrc.2010.12.065
M3 - Article
C2 - 21172305
AN - SCOPUS:78751612003
SN - 0006-291X
VL - 404
SP - 809
EP - 815
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -
