ArticleAging2010
DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence.
Article in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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Who cites it
121 citing papers in PubMed, 156 citations in OpenAlex.
- Regulation of ribosomal gene expression and senescence by a PML-mTOR-RONIN nuclear complex in triple-negative breast cancer.Oncogene · 2025Article
- Atrial myocyte senescence as a driver of atrial fibrillation: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Genome homeostasis defects drive enlarged cells into senescence.Molecular cell · 2023Article
- Single-cell transcriptomic analysis uncovers diverse and dynamic senescent cell populations.Aging · 2023Article
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- ROS-induced cell cycle arrest as a mechanism of resistance in polyaneuploid cancer cells (PACCs).Progress in biophysics and molecular biology · 2021Article
- Anti-aging: senolytics or gerostatics (unconventional view).Oncotarget · 2021Review
- Molecular mechanisms and cardiovascular implications of cancer therapy-induced senescence.Pharmacology & therapeutics · 2021Review
- Translational Control during Cellular Senescence.Molecular and cellular biology · 2021Review
- Counteracting CAR T cell dysfunction.Oncogene · 2021Review
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- Regulation of senescence traits by MAPKs.GeroScience · 2020Review
- Proteostasis failure and cellular senescence in long-term cultured postmitotic rat neurons.Aging cell · 2020Article
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- Moderate hyperoxia induces senescence in developing human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Apoptotic Effects of Drug Targeting Conjugates Containing Different GnRH Analogs on Colon Carcinoma Cells.International journal of molecular sciences · 2019Article
- Is cellular senescence involved in cystic fibrosis?Respiratory research · 2019Review
- Loss of the ubiquitin conjugating enzyme UBE2E3 induces cellular senescence.Redox biology · 2018Article
61 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When the cell cycle is arrested, growth-promoting pathways such as mTOR (Target of Rapamycin) drive cellular senescence, characterized by cellular hyper-activation, hypertrophy and permanent loss of the proliferative potential. While arresting cell cycle, p53 (under certain conditions) can inhibit the mTOR pathway. Senescence occurs when p53 fails to inhibit mTOR. Low concentrations of DNA-damaging drugs induce p53 at levels that do not inhibit mTOR, thus causing senescence. In quiescence caused by serum starvation, mTOR is deactivated. This predicts that induction of p53 will not cause senescence in such quiescent cells. Here we tested this prediction. In proliferating normal cells, etoposide caused senescence (cells could not resume proliferation after removal of etoposide). Serum starvation prevented induction of senescence, but not of p53, by etoposide. When etoposide was removed, such cells resumed proliferation upon addition of serum. Also, doxorubicin did not cause senescent morphology in the absence of serum. Re-addition of serum caused mTOR-dependent senescence in the presence of etoposide or doxorubicin. Also, serum-starvation prevented senescent morphology caused by nutlin-3a in MCF-7 and Mel-10 cells. We conclude that induction of p53 does not activate the senescence program in quiescent cells. In cells with induced p53, re-activation of mTOR by serum stimulation causes senescence, as an equivalent of cellular growth.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.