Metabolic Pathways Regulating Colorectal Cancer Initiation and Progression
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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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KRAS mutant colorectal cancer harbors boosted glucose metabolism and deregulation of glutamine, amino-acid, and fatty acid metabolism that support cancer cell proliferation.
“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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MASS SPECTROMETRY‐BASED MITOCHONDRIAL PROTEOMICS IN HUMAN OVARIAN CANCERS
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Myelodysplastic Syndromes and Metabolism
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- 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 · 2019: 5
- 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
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