The DOI matches its Crossref record; 105 of the 105 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Jemal, A., Bray, F., Ferlay, J., Ward, E., & Forman, D. (2011) · CA A Cancer Journal for Clinicians · doi:10.3322/caac.20107 · Cited by 55,077
Global cancer statistics, 2012
Torre, L. A., Bray, F., Siegel, R. L., Ferlay, J., Lortet‐Tieulent, J., & Jemal, A. (2015) · CA A Cancer Journal for Clinicians · doi:10.3322/caac.21262 · Cited by 27,235
A genetic model for colorectal tumorigenesis
Fearon, E. R., & Vogelstein, B. (1990) · Cell · doi:10.1016/0092-8674(90)90186-i · Cited by 12,132
Comprehensive molecular characterization of human colon and rectal cancer
The Cancer Genome Atlas Network (2012) · Nature · doi:10.1038/nature11252 · Cited by 8,499
The emerging hallmarks of cancer metabolism
Pavlova, N. N., & Thompson, C. B. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.12.006 · Cited by 5,926
Identification of stem cells in small intestine and colon by marker gene Lgr5
Barker, N., van Es, J. H., Kuipers, J., Kujala, P., van den Born, M., Cozijnsen, M., Haegebarth, A., Korving, J., Begthel, H., Peters, P. J., et al. (2007) · Nature · doi:10.1038/nature06196 · Cited by 5,687
Cancer incidence and mortality patterns in Europe: Estimates for 40 countries in 2012
Ferlay, J., Steliarova‐Foucher, E., Lortet‐Tieulent, J., Rosso, S., Coebergh, J. W. W., Comber, H., Forman, D., & Bray, F. (2013) · European Journal of Cancer · doi:10.1016/j.ejca.2012.12.027 · Cited by 5,243
The consensus molecular subtypes of colorectal cancer
Guinney, J., Dienstmann, R., Wang, X., de Reyniès, A., Schlicker, A., Soneson, C., Marisa, L., Roepman, P., Nyamundanda, G., Angelino, P., et al. (2015) · Nature Medicine · doi:10.1038/nm.3967 · Cited by 5,170
Lessons from hereditary colorectal cancer
Kinzler, K. W., & Vogelstein, B. (1996) · Cell · doi:10.1016/s0092-8674(00)81333-1 · Cited by 4,919
Identification and expansion of human colon-cancer-initiating cells
Ricci‐Vitiani, L., Lombardi, D. G., Pilozzi, E., Biffoni, M., Todaro, M., Peschle, C., & Maria, R. D. (2006) · Nature · doi:10.1038/nature05384 · Cited by 4,001
Cited by
Sorted by citations
Sepsis-induced immunosuppression: mechanisms, diagnosis and current treatment options
Liu, D., Huang, S., Sun, J., Zhang, H., Cai, Q., Gao, C., Li, L., Cao, J., Xu, F., Zhou, Y., et al. (2022) · Military Medical Research · doi:10.1186/s40779-022-00422-y · Cited by 646
Colorectal Cancer: Epidemiology, Risk Factors, and Prevention
Roshandel, G., Ghasemi‐Kebria, F., & Malekzadeh, R. (2024) · Cancers · doi:10.3390/cancers16081530 · Cited by 476
Stefani, C., Miricescu, D., Stanescu-Spinu, I.-I., Nica, R. I., Greabu, M., Totan, A. R., & Jinga, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221910260 · Cited by 402
Abedizadeh, R., Majidi, F., Khorasani, H. R., Abedi, H., & Sabour, D. (2023) · Cancer and Metastasis Reviews · doi:10.1007/s10555-023-10158-3 · Cited by 336
Insulin-Like Growth Factor 1 (IGF-1) Signaling in Glucose Metabolism in Colorectal Cancer
Kasprzak, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126434 · Cited by 248
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 ›
Are you an author, or do you see a problem with this page? Request a review
