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p21 in Cancer Research
Open accessAbstract
p21 functions as a cell cycle inhibitor and anti-proliferative effector in normal cells, and is dysregulated in some cancers. Earlier observations on p21 knockout models emphasized the role of this protein in cell cycle arrest under the p53 transcription factor activity. Although tumor-suppressor function of p21 is the most studied aspect of this protein in cancer, the role of p21 in phenotypic plasticity and its oncogenic/anti-apoptotic function, depending on p21 subcellular localization and p53 status, have been under scrutiny recently. Basic science and translational studies use precision gene editing to manipulate p21 itself, and proteins that interact with it; these studies have led to regulatory/functional/drug sensitivity discoveries as well as therapeutic approaches in cancer field. In this review, we will focus on targeting p21 in cancer research and its potential in providing novel therapies.
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“Of note, 38-50% of human cancers carry inactivating alterations in TP53 (ref. 132 ) , 48-80% in CDKN2A 133 and 14% in CIP1 (ref. 134 ) , while 15-20% and up to 8% harbour oncogenic mutations in RAS and BRAF , respectively 135,136 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [134]
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Metadata
- Authors
- Shamloo, B., & Usluer, S.
- Affiliations
- University of Utah (US)
- Medical University of Graz (AT)
- Corresponding author
- Shamloo, Bahar
- Venue
- Cancers
- Publisher
- MDPI AG
- Published
- 2019-08-14
- Volume
- 11
- Issue
- 8
- Pages
- 1178
- ISSN
- 2072-6694 (ISSN-L)
- PMC
- PMC6721478
- OpenAlex
- W2968190332
- Cited by
- 336
- References
- 175
- Citations by year
- 2026: 18 · 2025: 47 · 2024: 63 · 2023: 65 · 2022: 52 · 2021: 56 · 2020: 31 · 2019: 3
- FWCI
- 3.41
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancers (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- 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 › Ubiquitin and proteasome pathways
- Keywords
- p21, cell cycle inhibitors, p53, tumor suppression, phenotypic plasticity, oncogenic function, anti-apoptotic effects, subcellular localization, genome editing, cancer therapy, drug sensitivity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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