| External factors: | Nutlin-3 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Renal carcinoma |
| Experiment: | SA-β-gal activity assay//Flow cytometry |
| Description: | The observed inhibition of proliferation in p53 wild-type cells is due to a reduction in S-phase, indicated by measuring BrdU incorporation. This is indicative of G1 arrest, as expected for cells in which p53 activity has been rescued through inhibition of MDM2 binding with Nutlin-3 [26]. It is noteworthy that we have not observed evidence of apoptosis in RCC cells treated with Nutlin-3. This observation accords with recent studies demonstrating that Nutlin-3 can induce cell cycle arrest in RCC cells [27].We therefore examined senescence in RCC cells exposed to Nutlin-3 , a significant increase in senescence in cells expressing wild-type, but not mutant p53, as indicated by measurements of senescence-associated (SA) β-galactosidase, was detected. |
| Target gene: | P53//MDM2//P21 |
| R-EF-Target gene: | Upregulation//Upregulation//Upregulation |
| Official symbol(s): | P53//MDM2//P21 |
| Target gene experiment: | Western blot |
| Target gene description: | Treatment of RCC cells with Nutlin-3 leads to increased expression of p53 and some p53 target genes: MDM2, and p21 (CDKN1A). |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: