Human Gene Set: OUYANG_PROSTATE_CANCER_PROGRESSION_DN

For the Mouse gene set with the same name, see OUYANG_PROSTATE_CANCER_PROGRESSION_DN

Standard name OUYANG_PROSTATE_CANCER_PROGRESSION_DN
Systematic name M14636
Brief description Genes down-regulated during prostate cancer progression in mice heterozygotic for both NKX3.1 and PTEN [GeneID=4824;5728].
Full description or abstract To identify biomarkers that discriminate the aggressive forms of prostate cancer, we performed gene expression profiling of prostate tumors using a genetically engineered mouse model that recapitulates the stages of human prostate cancer, namely Nkx3.1; Pten mutant mice. We observed a significant deregulation of the epidermal growth factor and mitogen-activated protein kinase (MAPK) signaling pathways, as well as their major downstream effectors--the activator protein-1 transcription factors c-Fos and c-Jun. Forced expression of c-Fos and c-Jun in prostate cancer cells promotes tumorigenicity and results in activation of extracellular signal-regulated kinase (Erk) MAPK signaling. In human prostate cancer, up-regulation of c-Fos and c-Jun proteins occurs in advanced disease and is correlated with Erk MAPK pathway activation, whereas high levels of c-Jun expression are associated with disease recurrence. Our analyses reveal a hitherto unappreciated role for AP-1 transcription factors in prostate cancer progression and identify c-Jun as a marker of high-risk prostate cancer. This study provides a striking example of how accurate mouse models can provide insights on molecular processes involved in progression and recurrence of human cancer.
Collection C2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 18381418   Authors: Ouyang X,Jessen WJ,Al-Ahmadie H,Serio AM,Lin Y,Shih WJ,Reuter VE,Scardino PT,Shen MM,Aronow BJ,Vickers AJ,Gerald WL,Abate-Shen C
Exact source Table 1: Fold change < 0
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Source species Mus musculus
Contributed by Jessica Robertson (MSigDB Team)
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AFFY_Mouse430
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Version history 3.0: First introduced

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