| External factors: | ST1968 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Cancer |
| Experiment: | SA-β-gal activity assay//Flow cytometry |
| Description: | Moreover, only in KB cells ST1968 produced a dose-dependent appearance of β-galactosidase-positive cells at 72 h following treatment. The emergence of a senescence phenotype likely reflected a persistent cell cycle arrest. Indeed, as previously reported [10], treatment of A2780 cells with ST1968 resulted in a moderate and time-dependent arrest in G2, but in a complete accumulation of KB cells in G2/M (around 90% at 72 h). |
| Regulatory pathway: | ATM-Chk2//ATR-Chk1 |
| R-EF-Pathway: | Activation//Activation |
| Official symbol(s): | ATM-CHEK2//ATR-CHEK1 |
| Pathway experiment: | Western blot//TUNEL assay |
| Pathway description: | Under these conditions the ATM inhibitor produced in A2780 cells an enhancement of the apoptosis induced by the camptothecin also supported by CPP32 cleavage. As expected the combination resulted in a substantial reduction of Chk2 phosphorylation at thr68.in KB cells the Chk1 inhibitor enhanced the ST1968-induced appearance of mitotic and apoptotic cells and almost completed eliminated the cells with senescence features. |
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