Structure and function of GC79/TRPS1, a novel androgen-repressible apoptosis gene

GTG Chang, GJCM van den Bemd, M Jhamai… - Apoptosis, 2002 - Springer
GTG Chang, GJCM van den Bemd, M Jhamai, AO Brinkmann
Apoptosis, 2002Springer
Expression of death-signaling genes induces many biochemical cascades resulting in
elimination of cells via apoptosis or programmed cell death. GC79/TRPS1 is a novel
apoptosis associated gene that encodes a multitype zinc finger GATA-type transcription
factor. Expression of GC79/TRPS1 is repressed in the rat ventral prostate and significantly
elevated after androgen withdrawal by castration. Castration leads to regression of the
prostate caused by apoptosis of androgen-dependent prostate cells. Prostate cancer …
Abstract
Expression of death-signaling genes induces many biochemical cascades resulting in elimination of cells via apoptosis or programmed cell death. GC79/TRPS1 is a novel apoptosis associated gene that encodes a multitype zinc finger GATA-type transcription factor. Expression of GC79/TRPS1 is repressed in the rat ventral prostate and significantly elevated after androgen withdrawal by castration. Castration leads to regression of the prostate caused by apoptosis of androgen-dependent prostate cells. Prostate cancer consists of androgen-dependent and androgen-independent cells. The androgen-independent cells, usually present in the prostate of advanced prostate cancer patients do not have the ability to undergo apoptosis after androgen withdrawal. GC79/TRPS1 expression in androgen-dependent prostate cancer cells is repressed by androgens, while GC79/TRPS1 expression is hardly detectable in androgen-independent prostate cancer cells under cell culture conditions. This suggests that lack of GC79/TRPS1 expression could be a mechanism for the inability to induce the apoptotic pathway in androgen-independent prostate cancer cells after androgen withdrawal. This review will focus on the current knowlegde of the structure and function of GC79/TRPS1, a novel androgen-repressible apoptosis gene.
Springer