DESCRIPTION:

Genes that are up-regulated after LAPC4 prostate cancer cells over-expressing the androgen receptor and treated with bicalutamide. The authors demonstrate that this leads to expression of AR-responsinve genes. The genes are from Supplemental figure 2 and represent genes upregulated2-fold with a p <0.05. The table was manually converted to HGNC identifiers by manual inspection to standardize gene representation. When several identifiers in supplemental figure 2 mapped to a single HGNC identifier, the identifier was only entered once.

LABEL:

Up-regulated by AR

SCORE TYPE:

Binary

DATE ADDED:

2018-03-20

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

Chen CD, Welsbie DS, Tran C, Baek SH, Chen R, Vessella R, Rosenfeld MG, Sawyers CL

TITLE:

Molecular determinants of resistance to antiandrogen therapy.

JOURNAL:

Nature medicine Jan 2004, Vol 10, pp. 33-9

ABSTRACT:

Using microarray-based profiling of isogenic prostate cancer xenograft models, we found that a modest increase in androgen receptor mRNA was the only change consistently associated with the development of resistance to antiandrogen therapy. This increase in androgen receptor mRNA and protein was both necessary and sufficient to convert prostate cancer growth from a hormone-sensitive to a hormone-refractory stage, and was dependent on a functional ligand-binding domain. Androgen receptor antagonists showed agonistic activity in cells with increased androgen receptor levels; this antagonist-agonist conversion was associated with alterations in the recruitment of coactivators and corepressors to the promoters of androgen receptor target genes. Increased levels of androgen receptor confer resistance to antiandrogens by amplifying signal output from low levels of residual ligand, and by altering the normal response to antagonists. These findings provide insight toward the design of new antiandrogens. PUBMED: 14702632
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