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Effects of Ca ++ mobilization on expression of androgen‐regulated genes: Interference with androgen receptor‐mediated transactivation by AP‐1 proteins
Author(s) -
Murtha Patricia E.,
Zhu Wen,
Zhang Jianye,
Zhang Shaobo,
Young Charles Y.F.
Publication year - 1997
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19971201)33:4<264::aid-pros7>3.0.co;2-h
Subject(s) - transactivation , androgen receptor , androgen , rna interference , gene , gene expression , receptor , mobilization , biology , cancer research , microbiology and biotechnology , endocrinology , medicine , chemistry , genetics , prostate cancer , cancer , hormone , history , rna , archaeology
Abstract BACKGROUND The adult prostate is maintained through an equilibrium between cell growth and death rates. Androgen deprivation induces an increase in intracellular Ca ++ , AP‐1 gene expression of androgen‐inducible genes. METHODS Northern blot analysis, band‐shift assays, and transient cotransfection assays were used to study the effects of Ca ++ mobilizer A23187 on gene expression in human prostate cancer cells. RESULTS A23187 repressed androgen‐upregulated mRNAs for prostate‐specific antigen (PSA) and hKLK2, and rapidly induced mRNA levels for c‐ fos and c‐ jun. AP‐1 protein‐DNA binding activities were elevated after A23187 treatments. Androgen receptor (AR)‐mediated induction of chloramphenicol acetyltransferase (CAT) reporter was repressed by AP‐1 proteins. CONCLUSIONS The repression of AR‐mediated induction of PSA and hKLK2 genes by Ca ++ mobilizers is due to the interference of AR transactivation activity by AP‐1 proteins. Prostate 33:264–270, 1997. © 1997 Wiley‐Liss, Inc.