| Gene name: | PROX1 |
| Aging type: | Accelerate |
| Aging characteristic: | Others |
| Tissue type: | Tumor tissue |
| Cell name: | HepG2,Hep3B,Mahlavu,SK-HEP-1 |
| Gene ID: | 5629 |
| Category: | protein coding |
| Phenotype: | Hepatocellular carcinoma |
| Experimental category: | HL |
| PMID: | 23291986 |
| Experiment: | BrdU assay//SA-β-gal activity assay//Western blot |
| Description: | We used SK-HEP-1 cells for overexpression study and found that Prox1 reduced proliferation (as indicated by BrdU incorporation) in a time-dependent manner with a 30% of inhibition was found at 72 h after Prox1 expression in these cells.we found that percentage of β-galactosidase-positive cells was significantly increased after Prox1 overexpression indicating an induction of senescence-like phenotype.we examined the expression of CDKI proteins in control and Prox1-overexpressing cells. Among these inhibitory proteins, only p53 was dramatically increased. |
| Target gene: | P53 |
| Official symbol(s): | P53 |
| R-AG-Target gene: | Upregulation |
| Subcategory: | Unclear |
| Target gene experiment: | Knockdown//SA-β-gal activity assay//Western blot |
| Target gene description: | We first demonstrated that increase of β-galactosidase-positive cells by Prox1 expression was totally abolished by knockdown of p53 by shRNA. Human telomerase reverse transcriptase (hTERT) and chemokine C-X-C motif ligand 1 (CXCL1) have been shown to be downregulated and upregulated separately by p53 during p53-mediated senescence. We found that Prox1 significantly repressed hTERT expression and this effect was abolished when p53 was inhibited by shRNA. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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