| Gene name: | AR |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | PC-3 |
| Gene ID: | 367 |
| Category: | protein coding |
| Phenotype: | Prostate cancer |
| Experimental category: | L |
| PMID: | 22403609 |
| Experiment: | Cell cycle analysis//SA-β-gal activity assay |
| Description: | Longterm AR activation resulted in G1 growth arrest; the cells assumed flattened vacuolized morphology, suggestive of either autophagy or senescence. The levels of the principal autophagy mediator Beclin-1 [23,28] remained stable in the presence of DHT pointing to senescence. SA-β-Gal positivity increased from the background 4% to nearly 40% in the presence of DHT (P,0.0002), suggesting senescence. |
| Target gene: | P53//P21//P63//RB |
| Official symbol(s): | P53//P21//TP63//RB |
| R-AG-Target gene: | --//Upregulation//Downregulation//-- |
| Subcategory: | Phosphorylation |
| Target gene experiment: | Knockdown//SA-β-gal activity assay//Western blot//RT-PCR |
| Target gene description: | PC-3 cells are p53 and p16 null, RWPE-1 cells are p53 and Rb null. LNCaP cells express wild-type p53, but its levels were unchanged by DHT exposure;p21 was critical for AR-induced senescence since p21 silencing significantly reduced SA-βGal-positive population after DHT-treatment cells;p21 knock-down increased p63 protein and mRNA.AR activation also caused p63 exclusion from the nuclei,suggesting that nuclear DNp63 is important for blocking senescence. .P63 deficit likely contributed to the AR-driven senescence, since p63 knock-down elevated senescence in parental PC-3 cells.In PC3-AR and LNCaP treated with DHT, Rb phosphorylation visibly diminished. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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