| Gene name: | CDK6 |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | BxPC-3,Panc-1,MiaPaCa-2 |
| Experiment: | SA-β-gal activity assay//EdU cell proliferation assay//Flow cytometry |
| Description: | The β-galactosidase assay was used to determine senescence following treatment with LEE011 and MEK162. Combined inhibition resulted in a significant increase in β-galactosidase staining when compared to monotherapy in all cell lines, suggesting that combined inhibition of CDK4/6 and MEK with LEE011 and MEK162, respectively, reduces proliferation through the induction of cellular senescence rather than through pro-apoptotic mechanisms in PDAC cell lines. In BxPC-3 cells, a significant decrease in proliferation was seen with individual treatment with LEE011 and MEK162 as well as the combination treatment. Compared to single-agent treatment, the combination of LEE011 and MEK162 resulted in a significant decrease in proliferation in Panc-1 and MiaPaCa-2 cells.In cell cycle analysis, BxPC-3, Panc-1 and MiaPaCa-2 cell lines displayed reduced S phase fraction and increased G0/G1 phase arrest, confirming inhibition of cell proliferation. |
| Target gene: | PERK |
| Official symbol(s): | EIF2AK3 |
| R-AG-Target gene: | Upregulation |
| Subcategory: | Phosphorylation |
| Target gene experiment: | Western blot |
| Target gene description: | We observed reduced phosphorylated ERK (pERK) levels at all doses and in a time-dependent manner. Finally, ctreatment with MEK162 and LEE011 alone and in combination resulted in suppressing both pERK and pRb levels in all cell lines. |
| Regulatory pathway: | -- |
| R-AG-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation:
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