Coordinated regulation of life and death by RB

Chau, B. Nelson; Wang, Jean Y.J.

doi:10.1038/nrc993

Cited by 292Cancer-related Molecular PathwaysCell death mechanisms and regulationPI3K/AKT/mTOR signaling in cancer

Coordinated regulation of life and death by RB

Chau, B. Nelson, Wang, Jean Y.J.·2003·Nature Reviews Cancer

DOI 10.1038/nrc993

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Abstract

Recent studies have shown that RB can inhibit apoptosis, independently of its ability to block cell proliferation. This poses the question of how cells choose to grow or to die when RB becomes inactivated. RB is phosphorylated following mitogenic stimulation, but it is degraded in response to death stimuli. Most sporadic cancers also inactivate RB by phosphorylation, rather than losing RB entirely--possibly to exploit the survival advantage conferred by RB under stress. Drawing from the different mechanisms of RB inactivation, we propose two models for ways in which cells use RB to make the choice of life versus death.

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Both p53/p21 and p16/pRB pathways are complex, involving many upstream regulators and downstream effectors along with varying side branches.
“Both these pathways are complex as they involve many upstream regulators and downstream effectors along with varying side branches (Chau and Wang, 2003; Levine and Oren, 2009).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Chau and Wang, 2003
Abnormal proliferation induced by loss of RB is often accompanied by increased cell death through p53-dependent and independent mechanisms.
“abnormal proliferation that is induced by loss of RB is often accompanied by increased cell death, through p53-dependent and independent mechanisms49,57,87–91.”
From Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008) · cites this paper as [88]

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Authors: Chau, B. N., & Wang, J. Y. J.
Affiliations: University of California San Diego (US)
Corresponding author: Wang, Jean Y.J.
ORCID: Wang, Jean Y.J.
Venue: Nature Reviews Cancer
Publisher: Springer Science and Business Media LLC
Published: 2003-02
Volume: 3
Issue: 2
Pages: 130-138
ISSN: 1474-175X (ISSN-L)
1474-1768
DOI: 10.1038/nrc993
OpenAlex: W1979104079
Cited by: 292
References: 64
Citations by year: 2025: 2 · 2024: 5 · 2023: 9 · 2022: 6 · 2021: 8 · 2020: 6 · 2019: 3 · 2018: 8 · 2017: 6 · 2016: 5 · 2015: 10 · 2014: 10 · 2013: 11 · 2012: 12
FWCI: 3.40
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Cancer (publishedVersion)
PubMed (publishedVersion)
Funders: Damon Runyon Cancer Research Foundation
National Cancer Institute (R01CA058320)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords: retinoblastoma protein, apoptosis, cell proliferation, retinoblastoma protein phosphorylation, mitogen stimulation, cancer survival, cell fate determination, Rb inactivation
MeSH terms: Animals, Cell Cycle, Cell Survival, Humans, Neoplasms, Retinoblastoma Protein, Apoptosis, Mice, Knockout, Mice

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