ArticleFrontiers in pharmacology2021
Targeting Fatty Acid Synthase Modulates Metabolic Pathways and Inhibits Cholangiocarcinoma Cell Progression.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Aberrant Energy Metabolism in Tumors and Potential Therapeutic Targets.Genes, chromosomes & cancer · 2024Pooled it
- PUF, a biflavone monomer, triggers DNA damage through SLC25A15 downregulation and purine metabolic suppression in DLBCL.Journal of translational medicine · 2026Article
- Beyond the convergence of metabolic reprogramming in primary liver cancer: a comprehensive review on energy and lipids metabolism.Frontiers in cell and developmental biology · 2026Review
- Metabolic Reprogramming-Targeted Therapeutic Strategies in Primary Liver Cancer: A Bibliometric and Visualized Analysis.Journal of hepatocellular carcinoma · 2026Article
- A novel lipid droplet-related prognostic signature reveals CIDEC as a key biomarker for pancreatic adenocarcinoma.Frontiers in oncology · 2026Article
- Cholangiocarcinoma cells direct fatty acids to support membrane synthesis and modulate macrophage phenotype.Hepatology communications · 2025Article
- Identification of serum metabolite biomarkers and metabolic reprogramming mechanisms to predict recurrence in cholangiocarcinoma.Scientific reports · 2025Article
- Reprogramming of fatty acid metabolism: a hidden force regulating the occurrence and progression of cholangiocarcinoma.Cell death discovery · 2025Review
- Investigating the causal relationship between the plasma lipidome and cholangiocarcinoma mediated by immune cells: a mediation Mendelian randomization study.Scientific reports · 2025Article
- Altered fatty acid metabolism rewires cholangiocarcinoma stemness features.JHEP reports : innovation in hepatology · 2024Article
- MAL2 reprograms lipid metabolism in intrahepatic cholangiocarcinoma via EGFR/SREBP-1 pathway based on single-cell RNA sequencing.Cell death & disease · 2024Article
- Fatty acid synthase (FASN) signalome: A molecular guide for precision oncology.Molecular oncology · 2024Article
- Metabolic reprogramming in the tumor microenvironment of liver cancer.Journal of hematology & oncology · 2024Review
- Transcending frontiers in prostate cancer: the role of oncometabolites on epigenetic regulation, CSCs, and tumor microenvironment to identify new therapeutic strategies.Cell communication and signaling : CCS · 2024Review
- The role of metabolic reprogramming in liver cancer and its clinical perspectives.Frontiers in oncology · 2024Review
- Targeting dysregulated lipid metabolism in the tumor microenvironment.Archives of pharmacal research · 2023Review
- Identification of potential bioactive compounds ofBiochemistry and biophysics reports · 2023Article
- Targeting Oncometabolites in Peritoneal Cancers: Preclinical Insights and Therapeutic Strategies.Metabolites · 2023Review
- CircRNA MBOAT2 promotes intrahepatic cholangiocarcinoma progression and lipid metabolism reprogramming by stabilizing PTBP1 to facilitate FASN mRNA cytoplasmic export.Cell death & disease · 2023Article
- Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An aberrant regulation of lipid metabolism is involved in the pathogenesis and progression of cancer. Up-regulation of lipid biosynthesis enzymes, including acetyl-CoA carboxylase (ACC), fatty acid synthase (FASN) and HMG-CoA reductase (HMGCR), has been reported in many cancers. Therefore, elucidating lipid metabolism changes in cancer is essential for the development of novel therapeutic targets for various human cancers. The current study aimed to identify the abnormal expression of lipid-metabolizing enzymes in cholangiocarcinoma (CCA) and to evaluate whether they can be used as the targets for CCA treatment. Our study demonstrated that a high expression of FASN was significantly correlated with the advanced stage in CCA patients. In addition, survival analysis showed that high expression of FASN and HMGCR was correlated with shorter survival of CCA patients. Furthermore, FASN knockdown inhibited the growth, migration and invasion in CCA cell lines, KKU055 and KKU213, as well as induced cell cycle arrest and apoptosis in the CCA cell lines. In addition, metabolomics study further revealed that purine metabolism was the most relevant pathway involved in FASN knockdown. Adenosine diphosphate (ADP), glutamine and guanine levels significantly increased in KKU213 cells while guanine and xanthine levels remarkably increased in KKU055 cells showing a marked difference between the control and FASN knockdown groups. These findings provide new insights into the mechanisms associated with FASN knockdown in CCA cell lines and suggest that targeting FASN may serve as a novel CCA therapeutic strategy.
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