Gene Set: WANG_RESPONSE_TO_ANDROGEN_UP

Standard name WANG_RESPONSE_TO_ANDROGEN_UP
Systematic name M16075
Brief description Genes up-regulated in LNCaP cells (prostate cancer) treated with synthetic androgen R1881 [PubChem=13766].
Full description or abstract Progression of prostate cancer to androgen independence is suspected to involve the androgen and protein kinase A (PKA) signaling pathways. Here for the first time, the transcriptomes associated with each pathway and common transcriptional targets in response to stimulation of both pathways were identified in human prostate cancer cells using Affymetrix GeneChip technology (Human Genome U133 plus2). Statistically significant changes in the levels of 858 genes in response to androgen and 303 genes in response to activation of the PKA pathway were determined using GeneSpring software. Expression of a subset of these genes (22) that were transcriptional targets for the androgen and/or PKA pathways were validated by reverse transcriptase-polymerase chain reaction and Western blot analyses. Application of small interfering RNAs to the androgen receptor (AR) revealed that in addition to KLK3, levels of expression of KLK2 and SESN1 were regulated by AR activated by both the androgen and PKA signaling pathways. SESN1 was identified as a gene repressed by activated AR. These results provide a broad view of the effects of the androgen and PKA signaling pathways on the transcriptional program of prostate cancer cells and indicate that only a limited number of genes are targeted by cross-talk between AR and PKA pathways.
Collection C2: curated gene sets
      CGP: chemical and genetic perturbations
Source publication Pubmed 16751804   Authors: Wang G,Jones SJ,Marra MA,Sadar MD
Exact source Tables 1-3: Fold change in R1881 > 0
Related gene sets (show 2 additional gene sets from the source publication)

(show 7 gene sets from the same authors)
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Organism Homo sapiens
Contributed by Arthur Liberzon (MSigDB Team)
Source platform AFFY_HG_U133
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Version history 3.0: First introduced

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