| External factors: | Rapamycin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | ELISA |
| Description: | Rapamycin significantly decreased IL6 secretion by 3 strains of normal human fibroblasts, and 2 strains of immortal, but non-tumorigenic human breast epithelial cell lines (MCF-10A and 184A1)— all induced to senesce by ionizing radiation (10 Gy X-irradiation).Rapamycin also suppressed IL6 secretion by human fibroblasts induced to senesce by other stimuli. |
| Target gene: | IL1A |
| R-EF-Target gene: | Downregulation |
| Official symbol(s): | IL1A |
| Target gene experiment: | qPCR |
| Target gene description: | Rapamycin significantly decreased the translational efficiency of IL1A mRNA, and to a lesser extent IL1B, IL6 and IL8 mRNAs,in senescent cells. |
| Regulatory pathway: | mTOR//NF-κB |
| R-EF-Pathway: | --//Downregulation |
| Official symbol(s): | MTOR//NFKB1 |
| Pathway experiment: | Knockdown//ELISA//Luciferase reporter assay |
| Pathway description: | ShRNA against raptor, but not GFP, severely blunted IL6 secretion by senescent cells. Likewise, shRNA-mediated depletion of MTOR reduced senescence-associated IL6 secretion by >90% .We infected HCA2 cells with a lentivirus carrying an NF-κB–luciferase reporter, and measured the effect of rapamycin on reporter activity. Rapamycin reduced NF-κB activity by 80%. |
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