New plays in the p53 theater
Open accessAbstract
The p53 tumor suppressor and its paralogs p63 and p73 are at the crux of a network modulating cellular responses against potentially tumorigenic events. p53 acts primarily as a transcription factor, regulating the expression of both coding and non-coding RNAs, as well as the activity of RNA processing complexes. In line with their anti-tumorigenic function, p53 and p63 have recently been implicated in restricting tumor cell invasion. In parallel, a growing number of non-canonical target genes have been added to the p53 repertoire. These include genes encoding for proteins that impinge on a broad spectrum of cellular functions, from cell metabolism to stem cell renewal. The p53 story is still far from being fully told.
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A missense mutation in the p53 transcription factor can be held accountable for tumor initiation, development, and growth in more than half of solid tumor cancers.
“For instance, a missense mutation in the p53 transcription factor, which can be held accountable for tumor initiation, development, and growth in more than half of solid tumor cancers [32].”
From Microfluidic modelling of the tumor microenvironment for anti-cancer drug development (2019) · cites this paper as [32]
The Introduction (page unavailable) says p53 is mutated in approximately 50% of human cancers and describes its role in tumor prevention. The section on tumor cell invasion (page unavailable) says mutant p53 can promote cancer progression and metastasis. Neither passage establishes that the mutations are specifically missense mutations, that the figure exceeds half, or that it applies specifically to solid tumors. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe p53 protein acts as a tumor suppressor by inducing apoptosis when cellular mutations occur and initiating DNA repairs in healthy cells.
“Briefly, the p53 protein acts as a tumor suppressor as it induces apoptosis when cellular mutations occur and initiate DNA repairs in healthy cells [32].”
From Microfluidic modelling of the tumor microenvironment for anti-cancer drug development (2019) · cites this paper as [32]
The Introduction says that stress activates p53, which facilitates DNA repair and can instigate apoptosis; it also describes p53’s role in tumor prevention. It does not specifically say that mutations trigger apoptosis or distinguish DNA repair in healthy cells from repair in other cells. (LLM, conf=0.82)
Experimental — accuracy not yet measured
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- Authors
- Aylon, Y., & Oren, M.
- Affiliations
- Weizmann Institute of Science (IL)
- Corresponding author
- Oren, Moshe
- Venue
- Current Opinion in Genetics & Development
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 21
- Issue
- 1
- Pages
- 86-92
- ISSN
- 0959-437X (ISSN-L)
- PMC
- PMC3059112
- OpenAlex
- W1988733824
- Cited by
- 106
- References
- 63
- Citations by year
- 2025: 4 · 2024: 3 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 10 · 2019: 6 · 2018: 6 · 2017: 2 · 2016: 8 · 2015: 7 · 2014: 14 · 2013: 6 · 2012: 18
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Genetics & Development (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R37 CA40099, R37CA040099)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53, p63, p73, tumor suppressor, transcription factors, non-coding RNA, RNA processing, tumor invasion, cellular metabolism, stem cell self-renewal
- MeSH terms
- Animals, Humans, Neoplasms, Stem Cells, Signal Transduction, Tumor Suppressor Protein p53, RNA, Untranslated
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