论文部分内容阅读
目的:探讨自噬在TGF-β1调控EMT诱导头颈鳞癌侵袭转移中的作用。方法:不同浓度及时间点TGF-β1构建头颈鳞癌上皮-间质转化(EMT)模型,Western blot检测自噬相关蛋白LC3水平;自噬抑制剂氯喹(CQ)抑制自噬后,Western blot检测上皮细胞标志物钙黏蛋白、间质细胞标志物波形蛋白及LC3蛋白的表达;划痕、Transwell侵袭小室实验检测自噬对头颈鳞癌侵袭、转移的影响。结果:不同浓度及时间点TGF-β1诱导EMT的同时,诱导发生自噬,且随着TGF-β1浓度的增加及时间的延长,自噬随之增强;自噬被抑制后,E-cadherin表达上调、Vimentin表达下调,细胞迁移及侵袭潜能较对照组明显减弱。结论:TGF-β1诱导头颈鳞癌发生EMT的同时伴随自噬;自噬在TGF-β1调控头颈鳞癌EMT的过程中,能增强其侵袭、转移能力。
AIM: To investigate the role of autophagy in the regulation of EMT-induced invasion and metastasis of head and neck squamous carcinoma by TGF-β1. METHODS: Epithelial-mesenchymal transition (EMT) model of head and neck squamous cell carcinoma was established by TGF-β1 at different concentrations and time points. The level of autophagy-associated protein LC3 was detected by Western blot. After autophagy was inhibited by autophagy inhibitor chloroquine (CQ) Epithelial cell marker cadherin, interstitial cell marker vimentin and LC3 protein expression; scratch, Transwell invasive chamber experiments to detect the impact of autophagy on the invasion and metastasis of head and neck squamous cell carcinoma. Results: Autophagy was induced by TGF-β1 at different concentrations and time points, and the autophagy was enhanced with the increase of TGF-β1 concentration and time. E-cadherin expression was inhibited after autophagy was inhibited Upregulation, Vimentin expression down, cell migration and invasion potential was significantly weaker than the control group. Conclusion: TGF-β1 induces EMT accompanied with autophagy in squamous cell carcinoma of the head and neck. Autophagy can enhance the invasion and metastasis of TGF-β1 in the EMT of head and neck squamous cell carcinoma.