Regulation of cancer cell metabolism
Abstract
Interest in the topic of tumour metabolism has waxed and waned over the past century of cancer research. The early observations of Warburg and his contemporaries established that there are fundamental differences in the central metabolic pathways operating in malignant tissue. However, the initial hypotheses that were based on these observations proved inadequate to explain tumorigenesis, and the oncogene revolution pushed tumour metabolism to the margins of cancer research. In recent years, interest has been renewed as it has become clear that many of the signalling pathways that are affected by genetic mutations and the tumour microenvironment have a profound effect on core metabolism, making this topic once again one of the most intense areas of research in cancer biology.
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Cancer cells are often characterized by increased replication stress, altered DNA repair mechanisms or changes in chromatin structure.
“One possible explanation for the observed difference between cSNVs and dbSNVs could be system-wide alterations in cancer cells, which are often characterized by increased replication stress, altered DNA repair mechanisms or changes in chromatin structure (85,86).”
From G-quadruplex-mediated genomic instability drives SNVs in cancer (2024) · cites this paper as [85]
TME is implicated in induced metabolic rewiring in cancer cells.
“Recent findings implicate TME in the induced metabolic rewiring in cancer cells (Cairns et al., 2011; Fiaschi and Chiarugi, 2012; Rattigan et al., 2012).”
From Tumor microenvironment derived exosomes pleiotropically modulate cancer cell metabolism (2016) · cites this paper as Cairns et al., 2011
Cancer cells rely on aerobic glycolysis as their primary energy resource (the Warburg effect).
“Unlike normal cells, which derive most of their energy from mitochondrial oxidative phosphorylation, cancer cells rely on aerobic glycolysis as their primary energy resource. This process is recognized as the “Warburg effect”21–23.”
From RETRACTED ARTICLE: Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression (2020) · cites this paper as [22]
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- Authors
- Cairns, R. A., Harris, I. S., & Mak, T. W.
- Corresponding author
- Mak, Tak W.
- Venue
- Nature Reviews Cancer
- Published
- 2011-01-24
- Volume
- 11
- Issue
- 2
- Pages
- 85-95
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2028897202
- Semantic Scholar
- 9d36b5b10983f1aa90a9d9d5a7bcffe671b38257
- Cited by
- 4,744
- References
- 142
- Citations by year
- 2026: 95 · 2025: 192 · 2024: 234 · 2023: 276 · 2022: 293 · 2021: 418 · 2020: 423 · 2019: 386 · 2018: 386 · 2017: 414 · 2016: 399 · 2015: 387 · 2014: 318 · 2013: 251 · 2012: 192
- FWCI
- 19.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Keywords
- cancer metabolism, Warburg effect, redox homeostasis, tumor microenvironment, carcinogenesis, central metabolic pathways
- MeSH terms
- Cell Transformation, Neoplastic, Humans, Neoplasms, Oxidation-Reduction, Transcription Factors, Signal Transduction, Gene Expression Regulation, Neoplastic, Intracellular Signaling Peptides and Proteins, Gene Regulatory Networks
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