| Gene name: | CD9 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HUVEC |
| Gene ID: | 928 |
| Category: | protein coding |
| Phenotype: | Atherosclerosis |
| Experimental category: | HL |
| PMID: | 32346137 |
| Experiment: | Cell morphological analysis//BrdU assay//Flow cytometry//Immunostaining//SA-β-gal activity assay//Western blot |
| Description: | Young cells transduced with CD9 adenovirus were enlarged and flattened. Moreover, CD9 upregulation increased SAβG staining, but decreased BrdU incorporation, Ki67 immunoreactivity, the proportion of cells in the S phase, and endothelial tube formation. In addition, the levels of p53, p-p53, and p21 proteins increased. |
| Regulatory pathway: | PI3K-AKT-MTOR-P53 |
| R-AG-Pathway: | Activation |
| Official symbol(s): | PIK3CA-AKT1-MTOR-TP53 |
| Pathway experiment: | Knockdown//Western blot//SA-β-gal activity assay |
| Pathway description: | Pretreatment with LY294002, a specific inhibitor of PI3K [42], or rapamycin, an inhibitor of mTOR [43], reduced the levels of p53 and p21 and SAβG staining induced by CD9 overexpression. Knockdown of PIK3CA, but not that of PIK3CB, significantly decreased the levels of pAKT, p53, p-p53, pS6K, and p21 proteins, as well as SAβG staining, suggesting that PIK3CA might be involved in CD9- induced cellular senescence. These results indicate that the PI3K-AKT-mTOR-p53 pathway might regulate CD9- mediated cellular senescence. |
Annotation:
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