Gene Set: WANG_PROSTATE_CANCER_ANDROGEN_INDEPENDENT

Standard name WANG_PROSTATE_CANCER_ANDROGEN_INDEPENDENT
Systematic name M16347
Brief description Genes changed in prostate cancer: androgen independent vs androgen dependent samples.
Full description or abstract The androgen-signaling pathway plays an important role in the development and hormonal progression of prostate cancer to the castrate-resistant stage (also called androgen-independent or hormone refractory). The Wnt pathway and beta-catenin contribute to prostate biology and pathology. Here application of Affymetrix GeneChip analysis revealed the genomic similarity of the LNCaP hollow fiber model to clinical samples and identified genes with differential expression during hormonal progression. The fiber model samples clustered according to the expression profile of androgen-regulated genes to provide genomic evidence for the reactivation of the AR signaling pathway in castrate-resistant prostate cancer. Pathway-based characterization of gene expression identified activation of the Wnt pathway. Together with the increased expression of AR and beta-catenin, there was increased nuclear colocalization and interaction of endogenous AR and beta-catenin in castrate-resistant prostate cancer from castrated mice. Surprisingly, no interaction or colocalization of AR and beta-catenin could be detected in xenografts from noncastrated mice. These studies provide the first in vivo evidence to support aberrant activation of the AR through the Wnt/beta-catenin signaling pathway during progression of prostate cancer to the terminal castrate-resistant stage.
Collection C2: curated gene sets
      CGP: chemical and genetic perturbations
Source publication Pubmed 19047173   Authors: Wang G,Wang J,Sadar MD
Exact source Table 2S
Related gene sets (show 41 gene sets from the same authors)
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Organism Homo sapiens
Contributed by Jessica Robertson (Broad Institute)
Source platform HG-U133A
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Compendia expression profiles Human tissue compendium (Novartis)
NCI-60 cell lines (National Cancer Institute)
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Version history 3.0: First introduced

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