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Metabolic pathways regulating colorectal cancer initiation and progression
Open accessAbstract
Colorectal cancer (CRC) is one of the most common types of cancer worldwide. Despite recent advances in the molecular genetics of CRC, poor treatment outcomes highlight the need for a better understanding of the underlying mechanisms accounting for tumor initiation and progression. Recently, deregulation of cellular metabolism has emerged as a key hallmark of cancer. Reprogramming of core cellular metabolic pathways by cancer cells provides energy, anaplerotic precursors and reducing equivalents required to support tumor growth. Here, we review key findings implicating cancer metabolism as a major contributor of tumor initiation, growth and metastatic dissemination in CRC. We summarize the metabolic pathways governing stem cell fate in the intestine, the metabolic adaptations of proliferating colon cancer cells and their crosstalk with oncogenic signaling, and how they fulfill the energetic demands imposed by the metastatic cascade. Lastly, we discuss how some of these metabolic pathways could represent new vulnerabilities of CRC cells with the potential to be targeted.
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“Indeed, KRAS mutant CRC harbors a boosted glucose metabolism as well as deregulation of glutamine, amino-acid, and fatty acid metabolism that support cancer cell proliferation [48].”
From KRAS, a New Target for Precision Medicine in Colorectal Cancer? (2024) · cites this paper as [48]
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Metadata
- Authors
- La Vecchia, S., & Sebastián, C.
- Affiliations
- Candiolo Cancer Institute (IT)
- Corresponding author
- Sebastián, Carlos
- ORCID
- Sebastián, Carlos
- Venue
- Seminars in Cell & Developmental Biology
- Publisher
- Elsevier BV
- Published
- 2020-02
- Volume
- 98
- Pages
- 63-70
- ISSN
- 1084-9521 (ISSN-L)
- OpenAlex
- W2947351976
- Cited by
- 349
- References
- 105
- Citations by year
- 2026: 26 · 2025: 49 · 2024: 68 · 2023: 70 · 2022: 66 · 2021: 43 · 2020: 22
- FWCI
- 3.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Seminars in Cell and Developmental Biology (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- Funders
- FPRC 5 per mille 2011 MIUR
- FPRC 5 per mille 2014 MIUR
- RC 2018 Ministero della Salute
- European Union’s Horizon 2020 Research and Innovation Program (797464)
- 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 › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- colorectal cancer, cancer metabolism, tumor initiation, tumor progression, metabolic reprogramming, intestinal stem cells, colon cancer cells, oncogenic signaling, metastasis, metabolic vulnerability, therapeutic target
- MeSH terms
- Animals, Humans, Colorectal Neoplasms, Disease Progression, Metabolic Networks and Pathways, Cellular Reprogramming
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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