Cited by 40Telomeres, Telomerase, and SenescenceCancer, Hypoxia, and MetabolismGenetics, Aging, and Longevity in Model Organisms

Metabolic alterations accompanying oncogene-induced senescence

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Aird, Katherine M, Zhang, Rugang·2014·Molecular & Cellular Oncology

Abstract

Senescence is defined as a stable cell growth arrest. Oncogene-induced senescence (OIS) occurs in normal primary human cells after activation of an oncogene in the absence of other cooperating oncogenic stimuli. OIS is therefore considered a bona fide tumor suppression mechanism in vivo. Indeed, overcoming OIS-associated stable cell growth arrest can lead to tumorigenesis. Although cells that have undergone OIS do not replicate their DNA, they remain metabolically active. A number of recent studies report significant changes in cellular metabolism during OIS, including alterations in nucleotide, glucose, and mitochondrial metabolism and autophagy. These alterations may be necessary for stable senescence-associated cell growth arrest, and overcoming these shifts in metabolism may lead to tumorigenesis. This review highlights what is currently known about alterations in cellular metabolism during OIS and the implication of OIS-associated metabolic changes in cellular transformation and the development of cancer therapeutic strategies.

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Crossref · 10.4161/23723548.2014.963481

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  • During OIS, fatty acid metabolism is altered, glucose consumption is enhanced, and utilization of pyruvate in the tricarboxylic acid cycle and nucleotide deficiency are increased.

    “Moreover, during OIS, fatty acid metabolism is altered, glucose consumption is enhanced, and the utilization of pyruvate in the tricarboxylic acid cycle and nucleotide deficiency are increased [119,216,217,218,219].”

    From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [218]

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Authors
Aird, K. M., & Zhang, R.
Affiliations
The Wistar Institute (US)
Corresponding author
Aird, Katherine M
Venue
Molecular & Cellular Oncology
Published
2014-09-15
Volume
1
Issue
3
Pages
e963481
ISSN
  • 2372-3548 (ISSN-L)
  • 2372-3556
OpenAlex
W2018023609
Cited by
39
References
89
Citations by year
2025: 1 · 2024: 5 · 2023: 5 · 2022: 2 · 2021: 9 · 2020: 2 · 2019: 5 · 2018: 3 · 2017: 5 · 2016: 1 · 2015: 1
FWCI
0.27
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Molecular & Cellular Oncology (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
National Cancer Institute (T32CA009171)
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
oncogene-induced senescence, cellular metabolism, tumor suppression, growth arrest, nucleotide metabolism, glucose metabolism, mitochondrial metabolism, autophagy, cell transformation, carcinogenesis, cancer therapy

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