External factors
| External factors: |
Nutlin-3 |
| Category: |
Chemical compounds |
| Phenotype: |
Renal carcinoma |
| Cell name: |
ACHN,Caki-2,RCC |
| 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. |
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Regulatory relationship
| 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). |
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Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.
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