目的  探讨低氧通过乙酰辅酶A羧化酶1（ACC1）促进人肺腺癌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A549细胞的迁移（P＜0.01），低氧处理后ACC1表达上调（P＜0.01），同时波形蛋白（vimentin）表达增加（P＜0.05），E-钙黏蛋白（E-cadherin）表达下降（P＜0.01）；敲除ACC1后与对照组相比，A549细胞的迁移能力减弱（P＜0.05），vimentin表达下降（P＜0.05），E-cadherin表达增加（P＜0.01）；敲除ACC1后A549细胞在常氧和5％ O2条件下迁移数目及vimentin、E-cadherin表达变化无统计学意义（P＞0.05）；补充亚油酸（LA）恢复低氧对A549细胞的促迁移作用（P＜005）。   结论  低氧通过上调ACC1的表达促进肺腺癌A549细胞迁移及EMT转化。

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.