ArticleOncology letters2018
Upregulation of pyruvate kinase M2 expression by fatty acid synthase contributes to gemcitabine resistance in pancreatic cancer.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Prognosis After Curative Resection of Esophageal Basaloid Squamous Cell Carcinoma: A Single-Institution Retrospective Study.Annals of surgical oncology · 2026Article
- Orlistat potentiates the gemcitabine effect in inhibiting the malignant biological behavior of nasopharyngeal carcinoma by downregulating PKM2.Discover oncology · 2026Article
- PKM2 is a key regulator of cardiac lipid metabolism in mice.Mitochondrion · 2025Article
- Metabolic Reprogramming of Cancer Cells and Therapeutics Targeting Cancer Metabolism.Cancer medicine · 2025Review
- Fatty acid synthase (FASN) inhibition cooperates with BH3 mimetic drugs to overcome resistance to mitochondrial apoptosis in pancreatic cancer.Neoplasia (New York, N.Y.) · 2025Article
- Oncometabolites in pancreatic cancer: Strategies and its implications.World journal of experimental medicine · 2024Review
- Metformin Increases the Response of Cholangiocarcinoma Cells to Gemcitabine by Suppressing Pyruvate Kinase M2 to Activate Mitochondrial Apoptosis.Digestive diseases and sciences · 2024Article
- A stumbling block in pancreatic cancer treatment: drug resistance signaling networks.Frontiers in cell and developmental biology · 2024Review
- TRAF6 promotes chemoresistance to paclitaxel of triple negative breast cancer via regulating PKM2-mediated glycolysis.Cancer medicine · 2023Article
- Re-Shaping the Pancreatic Cancer Tumor Microenvironment: A New Role for the Metastasis Suppressor NDRG1.Cancers · 2023Review
- Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer.Acta biochimica et biophysica Sinica · 2023Review
- Lipid metabolism in pancreatic cancer: emerging roles and potential targets.Cancer communications (London, England) · 2022Review
- The role of metabolic reprogramming in pancreatic cancer chemoresistance.Frontiers in pharmacology · 2022Review
- Review
- MiR-486-3p was downregulated at microRNA profiling of adrenals of multiple endocrine neoplasia type 1 mice, and inhibited human adrenocortical carcinoma cell lines.Scientific reports · 2021Article
- Overcoming chemoresistance by targeting reprogrammed metabolism: the Achilles' heel of pancreatic ductal adenocarcinoma.Cellular and molecular life sciences : CMLS · 2021Review
- Altered glycolysis results in drug-resistant in clinical tumor therapy.Oncology letters · 2021Review
- Diagnostic Significance of Serum Fatty Acid Synthase in Patients with Pancreatic Cancer.Middle East journal of digestive diseases · 2021Article
- The Glycolytic Pathway as a Target for Novel Onco-Immunology Therapies in Pancreatic Cancer.Molecules (Basel, Switzerland) · 2021Review
- Stellate Cells Aid Growth-Permissive Metabolic Reprogramming and Promote Gemcitabine Chemoresistance in Pancreatic Cancer.Cancers · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer has one of the highest mortality rates of all cancer types. Fatty acid synthase (FASN) is a multifunctional protein homodimer that can convert acetyl coenzyme A (CoA) and malonyl-CoA into palmitate, thus regulating lipogenesis. FASN overexpression has also been shown to cause resistance to gemcitabine, a chemotherapy treatment for pancreatic cancer; however, the mechanism by which this happens is unclear. Analysis of gene expression of FASN and pyruvate kinase M2 (PKM2) in pancreatic cancer was performed using Oncomine microarray gene expression datasets, which demonstrated that FASN and PKM2 were upregulated in pancreatic cancer compared with normal tissue. Specifically, it was demonstrated that FASN enabled the upregulation of PKM2 expression at the mRNA and protein levels, increasing the glucose consumption rate in pancreatic cancer cells. The present study also revealed that decreased levels of FASN reduced resistance to gemcitabine treatment, which was induced by PKM2 overexpression in pancreatic ductal adenocarcinoma cells. Therefore, FASN may represent a novel therapeutic target in pancreatic cancer.
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