| Gene name: | PIM1 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | 22Rv1 |
| Experiment: | SA-β-gal activity assay//Cell morphological analysis |
| Description: | By the final passage (numbers 20–25), PIM1-expressing cells barely divided. The final-passage cells were found to have a flat and spread morphology and to be β-galactosidase (β-Gal) positive, consistent with the suggestion that they had undergone senescence. |
| Regulatory pathway: | P53-P21 |
| R-AG-Pathway: | Activation |
| Official symbol(s): | TP53-CDKN1A |
| Pathway experiment: | SA-β-gal activity assay//qRT-PCR//MTT assay//Western blot |
| Pathway description: | A marked change in the level of phosphorylation of these proteins occurs in late-passage PIM1-containing 22Rv1 cells and mirrors increases in the levels of the p21 protein . To examine the role of p21 in these cells, lentiviral vectors were used to transduce a Tet/ON-inducible shRNA directed at p21 (sh-p21) or a control sequence (sh-c) into 22Rv1 cells constitutively expressing PIM1 or a control vector. This shRNA was successful in decreasing p21 levels in control and PIM1-containing cells, but had no effect on the growth of 22Rv1 cells. In contrast, the growth of PIM1-containing 22Rv1 cells was markedly stimulated by decreasing the p21 levels. In these cells, decreased p21 levels correlated with a markedly lower level of γ-H2AX, staining of these late-passage PIM1–overexpressing cells with β-Gal shows that blocking p53 activity also prevents the induction of this marker of cell senescence by PIM1. |
Annotation:
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