| External factors: | AZD6738 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Colorectal cancer |
| Experiment: | SA-β-gal activity assay//Knockdown |
| Description: | Cells were treated with a highly selective ATR inhibitor, AZD6738.Compared to control cells, both RNASEH2B KO and RNASEH2A KO cells exhibited increased β-galactosidase staining , indicating that ATRi treatment accelerates cellular senescence in RNASEH2-depleted cells. |
| Regulatory pathway: | cGAS-STING |
| R-EF-Pathway: | Upregulation |
| Official symbol(s): | CGAS-STING1 |
| Pathway experiment: | qRT-PCR |
| Pathway description: | Expression levels of cGAS-STING target genes (e.g. IFN-β, ISG54 and CCL5) were higher in RNASEH2 deficient cells and could be further enhanced by ATRi treatment, which suggest the activation of cGAS-STING pathway may be another reason for increased cellular senescence caused by ATR inhibition. As it is reported that RNASEH2 deficiency could invoke cGAS-STING activation and because of the essential role of cGAS-STING pathway in cellular senescence30,31,56,57, we assume that the activation of cGAS-STING pathway may also contribute to senescence phenotype in our study. |
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