TY - JOUR
T1 - LEF1 in androgen-lndependent prostate cancer
T2 - regulation of androgen receptor expression, prostate cancer growth, and invasion
AU - Li, Yirong
AU - Wang, Longgui
AU - Zhang, Miao
AU - Melamed, Jonathan
AU - Liu, Xiaomei
AU - Reiter, Robert
AU - Wei, Jianjun
AU - Peng, Yi
AU - Zou, Xuanyi
AU - Pellicer, Angel
AU - Garabedian, Michael J.
AU - Ferrari, Anna
AU - Lee, Peng
PY - 2009/4/15
Y1 - 2009/4/15
N2 - A major obstacle in treating prostate cancer is the development of androgen-independent disease. In this study, we examined LEF1 expression in androgen-independent cancer as well as its regulation of androgen receptor (AR) expression, prostate cancer growth, and invasion in androgenindependent prostate cancer cells. Affymetrix microarray analysis of LNCaP and LNCaP-AI (androgen-independent variant LNCaP) cells revealed 100-fold increases in LEF1 expression in LNCaP-AI cells. We showed that LEF1 overexpression in LNCaP cells resulted in increased AR expression and consequently enhanced growth and invasion ability, whereas LEF1 knockdown in LNCaP-AI cells decreased AR expression and, subsequently, growth and invasion capacity. Chromatin immunoprecipitation, gel shift, and luciferase assays confirmed LEF1 occupancy and regulation of the AR promoter. Thus, we identified LEF1 as a potential marker for androgen-independent disease and as a key regulator of AR expression and prostate cancer growth and invasion. LEF1 is highly expressed in androgen-independent prostate cancer, potentially serving as a marker for androgen-independent disease.
AB - A major obstacle in treating prostate cancer is the development of androgen-independent disease. In this study, we examined LEF1 expression in androgen-independent cancer as well as its regulation of androgen receptor (AR) expression, prostate cancer growth, and invasion in androgenindependent prostate cancer cells. Affymetrix microarray analysis of LNCaP and LNCaP-AI (androgen-independent variant LNCaP) cells revealed 100-fold increases in LEF1 expression in LNCaP-AI cells. We showed that LEF1 overexpression in LNCaP cells resulted in increased AR expression and consequently enhanced growth and invasion ability, whereas LEF1 knockdown in LNCaP-AI cells decreased AR expression and, subsequently, growth and invasion capacity. Chromatin immunoprecipitation, gel shift, and luciferase assays confirmed LEF1 occupancy and regulation of the AR promoter. Thus, we identified LEF1 as a potential marker for androgen-independent disease and as a key regulator of AR expression and prostate cancer growth and invasion. LEF1 is highly expressed in androgen-independent prostate cancer, potentially serving as a marker for androgen-independent disease.
UR - http://www.scopus.com/inward/record.url?scp=65949084273&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=65949084273&partnerID=8YFLogxK
U2 - 10.1158/0008-5472.CAN-08-3380
DO - 10.1158/0008-5472.CAN-08-3380
M3 - Article
C2 - 19351848
AN - SCOPUS:65949084273
SN - 0008-5472
VL - 69
SP - 3332
EP - 3338
JO - Cancer Research
JF - Cancer Research
IS - 8
ER -
