MrgD通过抑制内质网应激调节肝癌细胞脂肪酸代谢

目的 抑制脂肪酸和胆固醇的合成可以有效降低肝癌细胞脂肪积累或脂质代谢,从而抑制肝细胞癌发生.本研究旨在探讨MrgD对肝癌细胞脂肪代谢的作用及机制.方法 借助慢病毒包装的重组MrgD表达质粒及MrgD干扰质粒,分别建立稳定性过表达和低表达MrgD的HepG2细胞株.利用游离脂肪酸诱导构建体外细胞脂肪变性模型,通过油红O染...

MrgD regulates fat acid metabolism in HepG2 via inhibiting ERS

Objective Inhibiting the synthesis of fatty acids and cholesterol could effectively reduce the occurrence of liver cancer, which is detrimental to the growth of hepatocarcinoma lesions. This study aims to explore the effect and mechanism of MrgD on the fat metabolism of hepatocyte. Methods The recombinant MrgD overexpression and interference plasmids were packaged by lentivirus to generate stable HepG2 cell lines with MrgD high and low expressions, respectively. In vitro steatosis model induced by free fatty acids, the effect of MrgD on HepG2 cells fatty acid metabolism was evaluated by oil red O staining, and fat synthesis-related genes （SREBP2, ACC1） and endoplasmic reticulum stress （ERS） marker protein （BiP） levels. Results The stable HepG2 cells with high or low expression of MrgD were successfully constructed. In the FFA-induced HepG2 cells, high MrgD expression significantly decreased the lipid droplet deposition and TG production compared with MrgD low expression. Meanwhile, MrgD overexpression inhibited the fat synthesis and ERS-related protein levels induced by fatty acids in HepG2 cells. Correspondingly, the expression levels of the fat synthesis and ERS-related proteins were significantly up-regulated in low-expressing MrgD HepG2 cells. Conclusion The study revealed that MrgD inhibits fat synthesis in hepatocarcinoma cells by regulating endoplasmic reticulum stress in vitro, suggesting that the MrgD pathway may be involved in developing hepatocellular carcinoma.