ArticleMediators of inflammation2023
High-Fat Mouse Model to Explore the Relationship between Abnormal Lipid Metabolism and Enolase in Pancreatic Cancer.
Article in Mediators of inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 8 citations in OpenAlex.
- Diagnostic value of miR-148b-3p in left ventricular hypertrophy patients with hypertension.BMC cardiovascular disorders · 2026Article
- Clinical characteristics of programmed death-1 inhibitors for older patients with advanced pancreatic cancer.World journal of gastrointestinal oncology · 2026Article
- ENO3 regulates ferroptosis by interaction with PKM2 to promote the progression of metabolic dysfunction-associated steatotic liver disease.Histology and histopathology · 2026Article
- HDL Cholesterol Levels and Pancreatic Cancer Risk: Protective Effects Revealed.Current cancer drug targets · 2026Article
- A deep learning-based prognostic prediction model for distal cholangiocarcinoma incorporating the metabolism-inflammation marker monocyte-to-high-density lipoprotein cholesterol ratio.Translational cancer research · 2025Article
- Nuclear magnetic resonance-based metabolomics and risk of pancreatic cancer: a prospective analysis in the UK Biobank.Journal of gastroenterology · 2025Article
- Genetic association of lipid-lowering drug target genes with pancreatic cancer: a Mendelian randomization study.Scientific reports · 2025Article
- Role of ENO1 and its targeted therapy in tumors.Journal of translational medicine · 2024Review
- Using machine learning to identify risk factors for pancreatic cancer: a retrospective cohort study of real-world data.Frontiers in pharmacology · 2024Article
- Monocyte to high-density lipoprotein ratio based prognostic nomogram for patients following allogeneic vascular replacement pancreaticoduodenectomy.Frontiers in genetics · 2024Article
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5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant tumors have become a major social health problem that seriously threatens human health, among which pancreatic cancer has a high degree of malignancy, difficult diagnosis and treatment, short survival time, and high mortality. More and more attention has been paid to abnormal lipid metabolism as a momentous carcinogenesis mechanism. Here, we explored the relationship between abnormal lipid metabolism, enolase, and pancreatic cancer by clinical data analysis. A high-fat mouse model was constructed, and then, a subcutaneous tumorigenesis mouse model of carcinoma of pancreatic cells and a metastatic neoplasm mouse pattern of pancreatic carcinoma cells injected through the tail vein were constructed to explore whether abnormal lipid metabolism affects the progression of pancreatic cancer in mice. We constructed a high-lipid model of pancreatic carcinoma cell lines and knockdown and overexpressed enolase in pancreatic carcinoma cell lines and investigated whether high lipid regulates epithelial-mesenchymal transition (EMT) by upregulating enolase (ENO), thereby promoting the cells of pancreatic carcinoma to invade and migrate. Triglycerides, total cholesterol, free cholesterin, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and neuron-specific enolase (NSE) from pancreatic cancer patients and nonpancreatic cancer patients were tested. The differences in blood lipids between patients with and without pancreatic carcinoma were compared, and the correlation between blood lipids and neuron-specific enolase was analyzed. We confirmed that the serum triglyceride level of pancreatic cancer patients at initial diagnosis is overtopping nonpancreatic cancer patients, and the neuron-specific enolase level of patients with pancreatic carcinoma is better than nonpancreatic carcinoma sufferers. Triglyceride level is positively correlated with neuron-specific enolase level, and serum triglyceride level has predictive value for pancreatic cancer. Hyperlipidemia can promote tumor growth and increase the expression levels of ENO1, ENO2, and ENO3 in subcutaneous tumor formation of pancreatic cancer in mice. Additional hyperlipidemia promoted pancreatic carcinoma metastasis in the lung in mice injected through the tail vein, which confirmed that hyperlipidemia accelerated the process of EMT by increasing the expression of ENO1, ENO2, and ENO3, therefore promoting the pancreatic cancer cell metastasis.
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