上皮-间质转化（EMT）是肿瘤迁移与侵袭的重要环节。近年来发现DEC1参与肿瘤EMT过程，但在不同肿瘤中作用不同，且具体机制不详。其在胃癌中的作用尚无研究报道。本课题前期工作发现胃癌中存在DEC1高表达；缺氧可诱导DEC1同时伴有EMT相关分子的表达；作为转录因子DEC1可能直接调节EMT相关分子的表达。综合大量文献及我们的前期工作，认为胃癌中常见的缺氧环境可诱导DEC1在胃癌细胞EMT过程中发挥重要作用。提出假说：缺氧可通过HIF-1α/DEC1/EMT和TGFβ/DEC1/EMT两条途径诱导胃癌细胞EMT。拟在胃癌中利用RNA干扰、基因过表达、TGFβR抑制剂等研究其分子机制，并建立裸鼠胃原位癌肿瘤模型进行体内研究。阐明DEC1在胃癌EMT中的作用及机制，可为寻找肿瘤治疗新靶点提供依据，同时也为肿瘤细胞内转录因子调控网络的信息完善积累资料。

Epithelial- mesenchymal transition（EMT）played a pivotal role in tumor migration and invasion proceeds. Recently, participation of DEC1 was disclosed in tumor EMT process, nevertheless its intimate mechanism was still opaque. Contributions of DEC1 in gastric cancer EMT have not been reported. Previous research of this issue demonstrated that DEC1 express abundantly in gastric cancer; hypoxic-induced DEC1 expression associated with EMT related molecular; as a transcript factor, DEC1 might regulate the expression of EMT related molecular. According published articles and our previous works, we presume that DEC1 plays a crucial role in hypoxic-induced EMT of gastric cancer cells. We hypothesized that Hypoxia induced EMT in gastric cancer through two pathways: HIF-1α/DEC1/EMT and TGFβ/DEC1/EMT. In this research, RNAi, Gene over-expression, TGFβR inhibition will be implemented for molecular mechanism investigation. Furthermore, in situ gastric tumor will be established using athymic mouse for researches in vivo. Elucidating function and mechanism of DEC1 in gastric cancer EMT, will bring evidences for the seeking of new tumor therapy targets, and accumulate information for transcript factors regulation networks.