| External factors: | Everolimus |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Eμ-Myc lymphoma |
| Experiment: | SA-β-gal activity assay//Western blot |
| Description: | Everolimus treatment was associated with robust acquisition of senescence-associated β-galactosidase (SA-β-gal) activity in tumors after 4 and 7 days of treatment that was lost upon disease relapse at day 11, indicating that they no longer retain the capacity to undergo senescence . Consistent with a senescence response, activation of the senescence regulatory kinase p38 mitogen-activated protein kinase (p38MAPK) occurred after 4 days of everolimus treatment ( 24 ). We also observed an increase in H3K9 trimethylation (H3K9me3), a chromatin marker of transcriptional silencing mechanistically linked to cellular senescence, likely through its role in directing the silencing of E2F target genes . We also observed a gene expression profile, including increased expression of transcripts encoding the extracellular signaling molecules ICAM1, IGFBP7, and interleukin (IL)-6 that is refl ective of a senescence response in B220 but not B220 cell populations in bone marrow isolated from mice treated for 4 days with everolimus . |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: