作者: Yuanqin Yin , Chengguang Sui , Fandong Meng , Ping Ma , Youhong Jiang
DOI: 10.1186/S12944-017-0474-X
关键词:
摘要: Docosahexaenoic acid(DHA) inhibits tumor growth and progression in various cancers, including lung cancer. However, the mechanisms involved remain unclear. The aim of this study was to identify mechanism DHA inhibiting non-small cell cancer (NSCLC) vitro. proliferation A549 tested by MTT, apoptosis analysed using flow cytometer. migration invasion were examined respectively wound healing assay Transwell assay. level ROS (reactive oxygen species, ROS) checked DCF (dichlorodihydrofluorescein, DCF) production cells. associated protein (caspase-3, PARP,Bax,Bcl-2 survivin) metastases proteins HEF1, MMP9 VEGF detected Western blot, same method used expression PI3K Akt. inhibited induced Moreover, it suppressed metastasis cells, while downregulating levels metastasis-associated proteins, matrix metallopeptidase (MMP9), vascular endothelial factor (VEGF), a dose -dependent manner. In addition, inactivated Akt phosphorylation. All these responses with accumulation intracellular ROS. downregulated antioxidant enzymes such as catalase, N-acetyl-cysteine (NAC) reversed effect DHA, which further validated our findings. present demonstrates that development tumors through an ROS-mediated inactivation PI3K/Akt signaling pathway.