ArticleCancers2023
Enhanced De Novo Lipid Synthesis Mediated by FASN Induces Chemoresistance in Colorectal Cancer.
Article in Cancers, 2023. 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 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed.
- Review
- Lipid metabolism as a central driver of immune remodeling and therapeutic vulnerability in metastatic colorectal cancer.Lipids in health and disease · 2026Review
- Fatty Acid Synthase as a Potential Metabolic Vulnerability in Ocular Adnexal Sebaceous Carcinoma.Cancers · 2026Article
- Correction: Han et al. Enhanced De Novo Lipid Synthesis Mediated by FASN Induces Chemoresistance in Colorectal Cancer.Cancers · 2025Article
- Targeting cancer metabolism: Therapeutic potential of the fatty acid synthase (FASN) inhibitors.Critical reviews in oncology/hematology · 2025Review
- Potential Application Value of FASN in the Diagnosis of Colorectal Cancer.JGH open : an open access journal of gastroenterology and hepatology · 2025Article
- Anoikis resistance in Cancer: Mechanisms, therapeutic strategies, potential targets, and models for enhanced understanding.Cancer letters · 2025Review
- Metabolic Adaptations in Cancer Progression: Optimization Strategies and Therapeutic Targets.Cancers · 2025Review
- The perspective of targeting cancer cell metabolism: combination therapy approaches.Molecular biology reports · 2025Review
- NAMPT Impairs Vascular Permeability in Periodontitis by Influencing FASN-mediated Lipogenesis.International journal of biological sciences · 2025Article
- Identification of lipid metabolism-related marker genes in colorectal cancer.American journal of cancer research · 2025Article
- PPARG Activation of Fatty Acid Metabolism Drives Resistance to Anti-HER2 Therapies in HER2-Positive Breast Cancer.International journal of biological sciences · 2025Article
- Metabolic Reprogramming in Colorectal Cancer: The Impact of Fatty Acid Metabolism.Human mutation · 2025Review
- Microbiota-host metabolism reprogramming in colorectal cancer: from pathogenesis to precision therapies.Frontiers in oncology · 2025Review
- Metabolic crossroads: unravelling immune cell dynamics in gastrointestinal cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Article
- Global research trends and prospects of cellular metabolism in colorectal cancer.World journal of gastrointestinal oncology · 2024Article
- Reprogrammed lipid metabolism in advanced resistant cancers: an upcoming therapeutic opportunity.Cancer drug resistance (Alhambra, Calif.) · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
backgroundOxaliplatin is one of the most widely used chemotherapy drugs for colorectal cancer (CRC). Resistance to oxaliplatin threatens the prognosis of CRC. Since previous studies have aroused interest in fatty acid metabolism in cancer, in this study, we determined whether fatty acid biosynthesis and the related regulating mechanism contribute to oxaliplatin resistance in CRC.
methodsThe effect of the fatty acid synthase (FASN) and its inhibitor Orlistat was characterized in Gene Expression Omnibus (GEO) databases, oxaliplatin-resistant cell lines, and xenografts. MRNA-seq and analysis identified related pathway changes after the application of Orlistat, which was verified by Western blotting.
resultsBy leveraging the GEO databases, FASN and closely related gene signatures were identified as being correlated with the response to oxaliplatin-based chemotherapy and poor prognosis. Additionally, FASN-upregulated expression promoted oxaliplatin resistance in CRC cell lines. We then applied Orlistat, a typical FASN inhibitor, in cell culture and xenograft models of oxaliplatin-resistant CRC, which attenuated the resistance to oxaliplatin. Additionally, the combination of the FASN inhibitor and oxaliplatin significantly increased cell cycle arrest and facilitated apoptosis, partly due to the diminished phosphorylation of the MAPK/ERK and PI3K/AKT pathways. In vivo studies showed that inhibiting fatty acid biosynthesis with Orlistat restrained the growth of xenograft tumors and increased the responsiveness to oxaliplatin.
conclusionsOur study revealed that FASN enhanced resistance to oxaliplatin in CRC. The inhibition of FASN could rescue the response to oxaliplatin by regulating MAPK/ERK and PI3K/AKT pathways.
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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.