ArticleThe Journal of clinical investigation2021
Enhanced triacylglycerol catabolism by carboxylesterase 1 promotes aggressive colorectal carcinoma.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
- Inhibiting menin attenuates high-fat diet-induced weight gain by limiting intestinal lipid absorption in mice.The Journal of clinical investigation · 2026Article
- Carboxylesterase 1 is a core metabolic vulnerability of platinum-resistant high-grade serous ovarian carcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Lipid metabolism reprogramming shapes the immune landscape in the tumor microenvironment.Cellular & molecular immunology · 2026Review
- Developing an isoflavone-based fluorescent probe for monitoring carboxylesterase on studying medicine-food homology samples.Analytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2026Article
- Microbial metabolic profiling reshapes NF-κB-mediated immune metabolic network: a new mechanism for CRC development.Journal of translational medicine · 2026Review
- NF-κB restrains nutrient-dependent transcription programs through chromatin modulation in Drosophila.Nucleic acids research · 2026Article
- Rosmarinic acid as a chemosensitizer in colorectal cancer: Targeting nuclear factor-kappa B pathway to overcome chemoresistance.World journal of clinical oncology · 2025Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Anticancer Activity of Roburic Acid: In Vitro and In Silico Investigation.International journal of molecular sciences · 2025Article
- Article
- Carboxylesterase 1-mediated endocannabinoid metabolism in skin: role in melanoma progression in BRafCancer & metabolism · 2025Article
- Impact of obesity and diabetes on colorectal cancer in Saudi Arabia is associated with liver γ‑glutamyl transferase abnormality.Experimental and therapeutic medicine · 2025Article
- Crosstalk between dysregulated amino acid sensing and glucose and lipid metabolism in colorectal cancer.Frontiers in oncology · 2025Review
- VPS37A Activates the Autophagy-Lysosomal Pathway for TNFR1 Degradation and Induces NF-Oncology research · 2025Article
- Hypercholesterolemia and the role of lipid metabolism gene CES1 in immune infiltration promote central nervous system relapse in acute myeloid leukemia.Frontiers in immunology · 2025Article
- Nicotine-induced CHRNA5 activation modulates CES1 expression, impacting head and neck squamous cell carcinoma recurrence and metastasis via MEK/ERK pathway.Cell death & disease · 2024Article
- NF-κB in biology and targeted therapy: new insights and translational implications.Signal transduction and targeted therapy · 2024Review
- NF-κB: Governing Macrophages in Cancer.Genes · 2024Review
- NF-κB signaling pathway in tumor microenvironment.Frontiers in immunology · 2024Review
- Unraveling the intricate relationship between lipid metabolism and oncogenic signaling pathways.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
27 authors at 8 institutions in 5 countries.
Funding
Abstract
The ability to adapt to low-nutrient microenvironments is essential for tumor cell survival and progression in solid cancers, such as colorectal carcinoma (CRC). Signaling by the NF-κB transcription factor pathway associates with advanced disease stages and shorter survival in patients with CRC. NF-κB has been shown to drive tumor-promoting inflammation, cancer cell survival, and intestinal epithelial cell (IEC) dedifferentiation in mouse models of CRC. However, whether NF-κB affects the metabolic adaptations that fuel aggressive disease in patients with CRC is unknown. Here, we identified carboxylesterase 1 (CES1) as an essential NF-κB-regulated lipase linking obesity-associated inflammation with fat metabolism and adaptation to energy stress in aggressive CRC. CES1 promoted CRC cell survival via cell-autonomous mechanisms that fuel fatty acid oxidation (FAO) and prevent the toxic build-up of triacylglycerols. We found that elevated CES1 expression correlated with worse outcomes in overweight patients with CRC. Accordingly, NF-κB drove CES1 expression in CRC consensus molecular subtype 4 (CMS4), which is associated with obesity, stemness, and inflammation. CES1 was also upregulated by gene amplifications of its transcriptional regulator HNF4A in CMS2 tumors, reinforcing its clinical relevance as a driver of CRC. This subtype-based distribution and unfavorable prognostic correlation distinguished CES1 from other intracellular triacylglycerol lipases and suggest CES1 could provide a route to treat aggressive CRC.
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Registered trials
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.