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.

中文翻译：

---

高脂小鼠模型探讨胰腺癌脂质代谢异常与烯醇化酶的关系

恶性肿瘤已成为严重威胁人类健康的重大社会健康问题，其中胰腺癌恶性程度高、诊治困难、生存时间短、死亡率高。脂质代谢异常作为一种重要的致癌机制越来越受到人们的关注。在这里，我们通过临床数据分析探讨脂质代谢异常、烯醇化酶与胰腺癌之间的关系。构建高脂小鼠模型，进而构建胰腺癌皮下致瘤小鼠模型和尾静脉注射胰腺癌细胞转移性肿瘤小鼠模型，探讨脂质代谢异常是否影响胰腺癌的进展。小鼠癌症。我们构建了胰腺癌细胞系的高脂模型，并在胰腺癌细胞系中敲低和过表达烯醇化酶，并研究高脂是否通过上调烯醇化酶（ENO）来调节上皮间质转化（EMT），从而促进胰腺癌细胞入侵和迁移。检测了胰腺癌患者和非胰腺癌患者的甘油三酯、总胆固醇、游离胆固醇、高密度脂蛋白胆固醇 (HDL-C)、低密度脂蛋白胆固醇 (LDL-C) 和神经元特异性烯醇化酶 (NSE)。比较胰腺癌患者与非胰腺癌患者血脂的差异，并分析血脂与神经元特异性烯醇化酶的相关性。我们证实，胰腺癌患者初诊时的血清甘油三酯水平高于非胰腺癌患者，并且胰腺癌患者的神经元特异性烯醇化酶水平优于非胰腺癌患者。甘油三酯水平与神经元特异性烯醇化酶水平呈正相关，血清甘油三酯水平对胰腺癌具有预测价值。高脂血症可促进小鼠胰腺癌皮下肿瘤形成中的肿瘤生长，并增加ENO1、ENO2、ENO3的表达水平。额外的高脂血症促进尾静脉注射小鼠的胰腺癌肺转移，证实高脂血症通过增加ENO1、ENO2和ENO3的表达加速EMT过程，从而促进胰腺癌细胞转移。