Oncogene-induced senescence: From biology to therapy

Zhu, Haoran; Blake, Shaun; Kusuma, Frances K; Pearson, Richard B; Kang, Jian; Chan, Keefe T

doi:10.1016/j.mad.2020.111229

Cited by 116Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsCancer-related Molecular Pathways

Oncogene-induced senescence: From biology to therapy

Zhu, Haoran, Blake, Shaun, Kusuma, Frances K, Pearson, Richard B, Kang, Jian, Chan, Keefe T·2020·Mechanisms of Ageing and Development

DOI 10.1016/j.mad.2020.111229

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Abstract

Oncogene-induced senescence (OIS) is a powerful intrinsic tumor-suppressive mechanism, arresting cell cycle progression upon oncogene-activating genomic alterations. The discovery and characterisation of the senescence-associated secretome unveiled a rich additional complexity to the senescence phenotype, including extrinsic impacts on the microenvironment and engagement of the immune response. Emerging evidence suggests that senescence phenotypes vary depending on the oncogenic stimulus. Therefore, understanding the mechanisms underlying OIS and how they are subverted in cancer will provide invaluable opportunities to identify alternative strategies for treating oncogene-driven cancers. In this review, we primarily discuss the key mechanisms governing OIS driven by the RAS/MAPK and PI3K/AKT pathways and how understanding the biology of senescent cells has uncovered new therapeutic possibilities to target cancer.

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Oncogene-induced senescence (OIS) is observed following the activation of various oncogenes such as B-RAFV600E or H-RAS G12V, as well as the loss of tumor suppressor proteins like PTEN or NF-1, in different cell types.
“Oncogene-induced senescence (OIS) is observed following the activation of various oncogenes such as B-RAFV600E or H-RAS G12V, as well as the loss of tumor suppressor proteins like PTEN or NF-1, in different cell types.284”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [284]
OIS is often associated with DNA replication stress and hyper-replication.
“OIS is often associated with DNA replication stress and hyper-replication.”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [284]

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Authors: Zhu, H., Blake, S., Kusuma, F. K., Pearson, R. B., Kang, J., & Chan, K. T.
Affiliations: Peter MacCallum Cancer Centre (AU)
The University of Melbourne (AU)
Corresponding author: Pearson, Richard B
Chan, Keefe T
ORCID: Zhu, Haoran
Kusuma, Frances K
Pearson, Richard B
Chan, Keefe T
Venue: Mechanisms of Ageing and Development
Publisher: Elsevier BV
Published: 2020-04
Volume: 187
Pages: 111229
ISSN: 0047-6374 (ISSN-L)
DOI: 10.1016/j.mad.2020.111229
OpenAlex: W3012052929
Semantic Scholar: fed4b9ce0f3a3d0ef55cdaf31e84387ee490b781
Cited by: 116
References: 136
Citations by year: 2026: 16 · 2025: 29 · 2024: 23 · 2023: 19 · 2022: 16 · 2021: 7 · 2020: 5 · 2014: 1
FWCI: 1.50
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Mechanisms of Ageing and Development (publishedVersion)
PubMed (publishedVersion)
Minerva Access (University of Melbourne) (submittedVersion)
Funders: Cancer Council Victoria (APP1065118)
Topics: Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords: oncogene-induced senescence, senescence-associated secretome, tumor suppression, RAS/MAPK pathway, PI3K/Akt signaling, tumor microenvironment, senescence therapy, cell cycle arrest
MeSH terms: Aging, Animals, Humans, Neoplasms, Oncogenes, Signal Transduction, Cellular Senescence, Tumor Microenvironment

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Oncogene-induced senescence: From biology to therapy

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