Cited by 338Cancer-related Molecular PathwaysPI3K/AKT/mTOR signaling in cancerUbiquitin and proteasome pathways

p21 in Cancer Research

Open access
Shamloo, Bahar, Usluer, Sinem·2019·Cancers

Abstract

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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Crossref · 10.3390/cancers11081178

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160 of 160 references verified0 citation errors · 0 not checkable

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  • 38-50% of human cancers carry inactivating alterations in TP53, 48-80% in CDKN2A and 14% in CIP1, while 15-20% and up to 8% harbour oncogenic mutations in RAS and BRAF, respectively.

    “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]

    The Discussion (section 5; page not provided) reports p21/CIP1 mutations in 14% of patients with invasive bladder cancer. It does not give that rate for human cancers generally or say that those mutations are inactivating. This verdict addresses the CIP1 figure to which this citation is attached, not the other genes cited separately. (LLM, conf=0.90)

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1 retracted

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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)
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 · 2018: 1
FWCI
3.41
Type
journal article
Language
en
Open access
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

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