ArticleOncogene2018
CPT1A-mediated fatty acid oxidation promotes colorectal cancer cell metastasis by inhibiting anoikis.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 252 papers.
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Who cites it
252 citing papers in PubMed, 378 citations in OpenAlex.
- Compartment-specific PPARδ activity controls the outcome of cancer-immune cell competition and immunotherapy efficacy.Nature immunology · 2026Article
- ALDH1B1 promotes mitochondrial γ-butyrobetaine biosynthesis and fatty acid oxidation in colorectal cancer.bioRxiv : the preprint server for biology · 2026Article
- Targeting colorectal cancer and T‑cell metabolism for the treatment of colorectal cancer (Review).Oncology reports · 2026Review
- Fatty acid metabolism in glioma: a review of novel targets and therapeutic strategies.Chinese neurosurgical journal · 2026Review
- Fatty Acid Metabolism and Hypoxia in the Tumor Microenvironment: Metabolic Adaptation and Clinical Potential in Colorectal Cancer.Biomedicines · 2026Review
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- Adipocytes in cancer a metabolic paradox and the dawn of novel therapeutics.Discover oncology · 2026Review
- Plasma proteome-metabolome signatures enable non-invasive early detection and lymph node risk stratification in breast cancer.Molecular cancer · 2026Article
- Review
- CTMP-REV7 axis modulates MHC-I antigen presentation via CDK1-AKT crosstalk in MSI-L/MSS colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- CPT1A loss promotes lung metastasis in immune-competent mice via a mechanism of mtDNA release and chronic activation of STING pathway.bioRxiv : the preprint server for biology · 2026Article
- Fatty acid metabolic reprogramming in the tumor microenvironment: Unraveling mechanisms and therapeutic prospects.Genes & diseases · 2026Review
- BPGM as an intrinsic brake to constrain metastasis through phospho-epigenetic-mediated carnitine biosynthesis suppression.Neoplasia (New York, N.Y.) · 2026Article
- Detachment-Induced FAK-STAT3-NNMT Inhibits CTCs Anoikis to Promote Breast Cancer Metastasis by Enhancing Fatty Acid Oxidation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Systemic Dyslipidemia Drives Pan-Cancer Prognosis via Epigenetic Remodeling: A Hybrid Pi-Score Analysis.Cancers · 2026Article
- Radiation-induced autophagy regulates fibroblast mitochondrial metabolism and crosstalk with triple-negative breast cancer cells.Cell reports · 2026Article
- Celecoxib suppresses colorectal cancer growth by inhibiting propionyl-CoA carboxylase alpha chain-mediated epithelial-mesenchymal transition and angiogenesis.Gastroenterology report · 2026Article
- SPIB suppresses protective autophagy via the IFIT2/PINK1/Parkin axis to promote anoikis in colorectal cancer.Cancer cell international · 2026Article
- A novel anoikis resistance-associated gene model for prognostic prediction and immune microenvironment characterization in lung squamous cell carcinoma.Discover oncology · 2026Article
- Proteogenomic Characterization Reveals Metabolic Vulnerabilities and Aberrant Phosphorylation in Colorectal Metastasis to Liver.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
192 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
22 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anoikis is a critical obstacle to cancer metastasis. Colorectal cancer (CRC) exhibits a high rate of metastasis, leading to death, and the mechanisms involved in anoikis resistance are still unclear. We identified that the fatty acid oxidation (FAO) pathway was activated in detached CRC cells. Multiple genes in the FAO pathway, specifically the rate-limiting enzyme CPT1A, were upregulated in CRC cells grown in suspension. Reactive oxygen species elimination mediated by CPT1A in CRC cells was vital to anoikis resistance. In vivo experiments showed that CPT1A-suppressed CRC cells colonized the lung at a much lower rate than normal CRC cells, suggesting that CPT1A-mediated FAO activation increased metastatic capacity. In clinical tissue specimens from CRC patients, elevated expression of CPT1A was observed in metastatic sites compared with primary sites. Our results demonstrate that CPT1A-mediated FAO activation induces CRC cells to resist anoikis, suggesting that CPT1A is an attractive target for treating metastatic CRC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.