ArticleLipids in health and disease2019
Inhibition of FASN suppresses the malignant biological behavior of non-small cell lung cancer cells via deregulating glucose metabolism and AKT/ERK pathway.
Article in Lipids in health and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 61 citations in OpenAlex.
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- METTL3 stabilizes FASN mRNA by mediating mCell & bioscience · 2026Article
- Targeted metabolism creates possibilities for lung cancer treatment in the precision tumor era.Respiratory research · 2026Review
- Bidirectional crosstalk between ER stress and lipid metabolism: From proteostasis to tumor adaptation.Cell death discovery · 2025Review
- Metabolic Heterogeneity Confers Differences in the Tumor Microenvironment of Aggressive Types of Melanomas.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2025Article
- PLA2 driven lipid signaling drives ARMS tumorigenic cell properties.Cell communication and signaling : CCS · 2025Article
- Lipid metabolic reprograming: the unsung hero in breast cancer progression and tumor microenvironment.Molecular cancer · 2025Review
- Fatty acid synthase in chemoresistance: mechanisms and therapeutic opportunities.Frontiers in pharmacology · 2025Review
- Metabolic reprogramming and therapeutic targeting in non-small cell lung cancer: emerging insights beyond the Warburg effect.Frontiers in oncology · 2025Review
- Elucidating the Role of FASN in Lung Cancer Stem Cells in Sensitive and Resistant EGFR-Mutated Non-Small Cell Lung Cancer Cells.Lung Cancer (Auckland, N.Z.) · 2025Article
- Fatty acid metabolism-derived prognostic model for lung adenocarcinoma: unraveling the link to survival and immune response.Frontiers in immunology · 2025Article
- The role of ESM1 in the lipids metabolic reprogramming and angiogenesis of lung adenocarcinoma cells.Heliyon · 2024Article
- Unravelling the Triad of Lung Cancer, Drug Resistance, and Metabolic Pathways.Diseases (Basel, Switzerland) · 2024Review
- Review
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- Epileptiform Discharges Reduce Neuronal ATP Production by Inhibiting F0F1-ATP Synthase Activity via A Zinc-α2-Glycoprotein-Dependent Mechanism.Molecular neurobiology · 2023Article
- Serum Insights: Leveraging the Power of miRNA Profiling as an Early Diagnostic Tool for Non-Small Cell Lung Cancer.Cancers · 2023Article
- A Systematic Role of Metabolomics, Metabolic Pathways, and Chemical Metabolism in Lung Cancer.Vaccines · 2023Review
- Lipids as Targets for Renal Cell Carcinoma Therapy.International journal of molecular sciences · 2023Review
- Applying machine learning algorithms to develop a survival prediction model for lung adenocarcinoma based on genes related to fatty acid metabolism.Frontiers in pharmacology · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFatty acid synthase (FASN) is overexpressed in most human carcinomas, including non-small cell lung cancer (NSCLC), and contributes to poor prognosis. An increasing number of studies have highlighted the potential function of FASN as both a biomarker and therapeutic target for cancers. However, the underlying molecular mechanisms of FASN in glucose metabolism and the malignant biological behavior of NSCLC remain the subjects of intensive investigation.
methodsFASN expression was depleted by FASN-siRNA in A549 and NCI-H1299 cell lines to detect the function of glucose metabolism and the malignant biological behavior of NSCLC cells. Western-blot and qPCR were applied to determine the expressions of FASN, t-AKT, p-AKT, t-ERK, p-ERK, PKM2, HK2 and AZGP1. ATP and lactate were detected to determine the activation of glucose metabolism. CCK8 and transwell assays were used to detect the proliferation, invasion, and migration capacity of the two types of NSCLC cells. The xenograft mouse model was used to evaluate tumor weights after suppression of FASN.
resultsLV-FASN-siRNA and its control lentiviral vector were successfully transfected into the two types of NSCLC cells (A549 and NCI-H1299). LV-FASN siRNA significantly suppressed FASN expression in both NSCLC cell types, and expressions of p-AKT, p-ERK, PKM2, and AZGP1 were also significantly decreased. Notably, the levels of ATP and lactate were significantly decreased after transfection with LV-FASN siRNA. The proliferation of both NSCLC cell types was decreased after suppression of FASN. The invasion and migration capacity of A549, but not NCI-H1299, were inhibited following down-regulation of FASN. In vivo, inhibition of FASN caused a marked animal tumor weight loss.
conclusionsFASN was involved in glucose metabolism via down-regulation of the AKT/ERK pathway and eventually altered the malignant phenotype in lung cancer cells.
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