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目的:探讨ω-3脂肪酸脱氢酶Fat-1基因对细胞脂肪酸谱的影响,并对AKT/Ras癌基因激活小鼠肝癌细胞的抑制作用。方法:通过构建p Lenti-CMV-Fat-1过表达慢病毒载体,使小鼠AKT/Ras肝癌细胞转染Fat-1基因,以p Lenti-CMV-GTP空载体病毒作为对照,观察Fat-1基因对小鼠AKT/Ras肝癌细胞增殖及克隆形成率的影响。Westernblot检测癌基因信号通路p-AKT和p-Erk的表达情况,并检测两组细胞脂肪酸谱的改变情况。结果:Fat-1基因可明显增加细胞ω-3/ω-6脂肪酸的比率,并抑制AKT/Ras癌基因信号通路,抑制肝癌细胞的增殖和克隆形成。结论:Fat-1基因通过增加内源性ω-3多不饱和脂肪酸来抑制AKT/Ras肝癌细胞的增殖。
Objective: To investigate the effect of Fat-1 gene of omega-3 fatty acid dehydrogenase on cell fatty acid profile and its inhibitory effect on hepatoma cells activated by AKT / Ras oncogene. Methods: Fat-1 gene was transfected into mouse AKT / Ras hepatocarcinoma cells by constructing p Lenti-CMV-Fat-1 overexpression lentiviral vector. The p Lenti-CMV-GTP empty vector was used as a control to observe the expression of Fat-1 Effects of Genes on Proliferation and Clone Formation of Mouse AKT / Ras Hepatoma Cells. Western blot was used to detect the expression of oncogene p-AKT and p-Erk, and the changes of cell fatty acid profiles were detected. Results: Fat-1 gene could significantly increase the ratio of omega-3 / omega-6 fatty acids and inhibit the AKT / Ras oncogene signaling pathway, and inhibit the proliferation and colony formation of hepatoma cells. Conclusion: Fat-1 gene inhibits the proliferation of AKT / Ras hepatocarcinoma cells by increasing endogenous ω-3 polyunsaturated fatty acids.