The promises and perils of p53
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In vitro, cellular senescence is a potent cell-autonomous barrier to OSKM transcription factor-mediated reprogramming, similar to its tumour suppressor role.
“In vitro studies demonstrated that cellular senescence is a potent cell-autonomous barrier for transcription factor-mediated reprograming using OCT4, SOX2, KLF4 and MYC (commonly referred to as OSKM), in a manner similar to its role in tumour suppression181–183.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [181]
The Abstract says that senescence may be a barrier to reprogramming in cultured cells and compares p53’s effects on reprogramming and tumour formation. But it says the senescence mechanism is suggested rather than demonstrated, and does not establish senescence specifically as a cell-autonomous barrier to OSKM-mediated reprogramming. (LLM, conf=0.84)
Experimental — accuracy not yet measuredActivation of p53 helps explain why induced pluripotent stem cells are produced only rarely during reprogramming.
“Recently we, and others, showed that p53 activation contributed to the low frequency of generating induced pluripotent stem cells (iPS) during cell reprogramming [79,80].”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [80]
Reducing p53 with shRNA makes cell reprogramming more efficient.
“Knocking down p53 by shRNA increased the efficiency of cell reprogramming.”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [80]
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References 16 · Cited by 274
Research works printed but not linked: 1
- [10]Banito A Genes Dev in the press
- Authors
- Krizhanovsky, V., & Lowe, S. W.
- Affiliations
- Howard Hughes Medical Institute (US)
- Venue
- Nature
- Published
- 2009-08
- Volume
- 460
- Issue
- 7259
- Pages
- 1085-1086
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2974062
- OpenAlex
- W1986832923
- Cited by
- 274
- References
- 16
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 6 · 2023: 3 · 2022: 4 · 2021: 13 · 2020: 13 · 2019: 9 · 2018: 16 · 2017: 20 · 2016: 18 · 2015: 10 · 2014: 20 · 2013: 27 · 2012: 30
- FWCI
- 14.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Cancer Institute (P01CA087497, P30CA008748)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- p53, induced pluripotent stem cells, tumour suppressor, p21, reprogramming efficiency, mouse embryonic fibroblasts, T cells, tumorigenicity, cancer stem cells, somatic cell reprogramming
- MeSH terms
- Animals, Cell Division, Fibroblasts, Humans, Neoplasms, Tumor Suppressor Protein p53, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Pluripotent Stem Cells, Mice, Cellular Reprogramming
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