p21 in cancer: Intricate networks and multiple activities

Abbas, Tarek; Dutta, Anindya

doi:10.1038/nrc2657

Cited by 2,712Cancer-related Molecular PathwaysSignaling Pathways in DiseasePI3K/AKT/mTOR signaling in cancer

p21 in cancer: Intricate networks and multiple activities

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Abbas, Tarek, Dutta, Anindya·2009·Nature Reviews Cancer

DOI 10.1038/nrc2657PMC PMC2722839

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Abstract

One of the main engines that drives cellular transformation is the loss of proper control of the mammalian cell cycle. The cyclin-dependent kinase inhibitor p21 (also known as p21WAF1/Cip1) promotes cell cycle arrest in response to many stimuli. It is well positioned to function as both a sensor and an effector of multiple anti-proliferative signals. This Review focuses on recent advances in our understanding of the regulation of p21 and its biological functions with emphasis on its p53-independent tumour suppressor activities and paradoxical tumour-promoting activities, and their implications in cancer.

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p21 is a potent cell-cycle inhibitor.
“p21 is a potent cell-cycle inhibitor (39)”
From Txnip Enhances Fitness of Dnmt3a -Mutant Hematopoietic Stem Cells via p21 (2022) · cites this paper as [39]
CDKN1A (p21, WAF1, CIP1) was among the first p53 target genes identified and is recognized as an encoder for a major cell cycle checkpoint control protein.
“CDKN1A (p21, WAF1, CIP1) was among the first p53 target genes11, 12 to be identified and is now recognized as an encoder for a major cell cycle checkpoint control protein.145”
From Census and evaluation of p53 target genes (2017) · cites this paper as [145]
p21 is rarely genetically affected in cancers.
“As p21 is rarely genetically affected in cancers [1,124]”
From CDK-Independent and PCNA-Dependent Functions of p21 in DNA Replication (2020) · cites this paper as [1]
Members of the Krüppel-like factor (KLF) transcription factor family can activate the CDKN1A gene by cooperating with p300-CREBBP.
“Members of the Krüppel-like factor (KLF) transcription factor (TF) family can activate the CDKN1A gene by cooperating with p300-CREBBP (Aliouat-Denis et al., 2005; Abbas and Dutta, 2009).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Abbas and Dutta, 2009
p21 can also be activated by p53 independent mechanisms by other stimulators such as nuclear receptors including androgen, vitamin D and retinoid receptors.
“p21WAF1/CIP1 can also be activated by p53 independent mechanisms by other stimulators such as nuclear receptors including androgen, vitamin D and retinoid receptors.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Abbas and Dutta, 2009

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Nuclear Receptor Hepatocyte Nuclear Factor 4α1 Competes with Oncoprotein c-Myc for Control of the p21/WAF1 Promoter
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Loss of the cell cycle inhibitors p21Cip1 and p27Kip1 enhances tumorigenesis in knockout mouse models
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Phosphorylation of the Cyclin-Dependent Kinase Inhibitor p21Cip1 on Serine 130 Is Essential for Viral Cyclin-Mediated Bypass of a p21Cip1-Imposed G1 Arrest
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High expression of p21WAF1/CIP1 is correlated with human hepatocellular carcinoma in patients with hepatitis C virus–associated chronic liver diseases
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Authors: Abbas, T., & Dutta, A.
Affiliations: University of Virginia (US)
Corresponding author: Abbas, Tarek
Dutta, Anindya
ORCID: Abbas, Tarek
Dutta, Anindya
Venue: Nature Reviews Cancer
Publisher: Springer Science and Business Media LLC
Published: 2009-05-14
Volume: 9
Issue: 6
Pages: 400-414
ISSN: 1474-175X (ISSN-L)
1474-1768
DOI: 10.1038/nrc2657
PMC: PMC2722839
OpenAlex: W2162262059
Cited by: 2,712
References: 236
Citations by year: 2026: 99 · 2025: 156 · 2024: 161 · 2023: 206 · 2022: 182 · 2021: 205 · 2020: 204 · 2019: 180 · 2018: 191 · 2017: 196 · 2016: 148 · 2015: 160 · 2014: 142 · 2013: 151 · 2012: 122
FWCI: 9.54
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Cancer (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Cancer Institute (R01CA089406, R01 CA 89406, T32CA009109)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords: p21, cyclin-dependent kinase inhibitors, cell cycle arrest, therapeutic target, cell transformation
MeSH terms: Animals, Cell Cycle, Humans, Neoplasms, Tumor Suppressor Protein p53, Cyclin-Dependent Kinase Inhibitor p21

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