低氧通过上调乙酰辅酶A羧化酶1促进肺腺癌A549细胞迁移

目的 探讨低氧通过乙酰辅酶A羧化酶1(ACC1)促进入肺腺癌A549细胞迁移的机制.方法 低氧(5％O2)处理肺腺癌A549细胞,应用Transwell迁移实验检测细胞迁移能力,Western blotting检测ACC1表达及上皮-间质转化(EMT)相关蛋白的表达水平.结果 与常氧(对照组)相比,低氧处理促进了A54...

Hypoxia promotes lung adenocarcinoma A549 cells migration by upregulating acetyl-CoA carboxylase 1

Objective To investigate the mechanism of hypoxia to promote human lung adenocarcinoma A549 cells migration through acetyl-CoA carboxylase 1 (ACC1). Methods Lung adenocarcinoma A549 cells were treated with hypoxia (5% O₂). Transwell migration assay was used to detect cell migration ability. Western blotting was used to detect ACC1 expression and epithelial-mesenchymal transition (EMT) related protein expression. Results Compared with the normoxia (control group), hypoxia treatment promoted the migration of A549 cells (P<0.01), ACC1 expression was up-regulated after hypoxia treatment (P<0.01), and vimentin expression was detected to increase significantly (P<0.05), E-cadherin expression decreased (P<0.01); Compared with the control group, migration of A549 cells was inhibited (P<0.05), vimentin expression was down-regulated (P<0.05), and E-cadherin expression increased after knocking down ACC1(P<0.01). After ACC1 was knocked down, the differences between the numbers of migration of A549 cells under normoxia and 5% O2 conditions and the expressions of vimentin and E-cadherin were not statistically significant (P>0.05). After linoleic acid (LA) supplementation, the hypoxia-induced migration promotion of A549 cells was restored. Conclusion Hypoxia can promote the migration and EMT transformation of lung adenocarcinoma A549 cells by up-regulating the expression of ACC1.