胃癌是最常见的恶性肿瘤之一，其致死率高而治愈率低，对于胃癌进展的分子机制还需要更加深入的研究。我们的前期研究发现GAGE7B在胃癌中高表达并且可促进胃癌细胞转移和增殖，但其异常高表达的分子机制尚不清楚。我们首先确定了GAGE7B的核心启动子，预测并发现转录因子YY1和c-Myc可上调GAGE7B的表达。c-Myc可直接结合GAGE7B启动子并上调GAGE7B表达，但未检测到YY1结合GAGE7B启动子。有趣的是，c-Myc启动子区还存在YY1潜在的结合位点，提示YY1可能通过调控c-Myc进而间接调节GAGE7B表达。胃癌细胞中YY1对GAGE7B表达的调控机制是本项目研究的重要内容之一。后续还将探讨YY通过调控c-Myc介导的GAGE7B高表达对胃癌进展的调控。本项目对深入探讨GAGE7B异常高表达的调控机制，及其通过调控GAGE7B促进胃癌进展的机制有着重要意义。

Gastric cancer is one of the most common malignancies and one of the most common causes of cancer-related mortality. The progression of gastric cancer should be deeply studied especially at molecular level. GAGE7B was found to be upregulated in gastric cancer and could promote the cancer cells' migration and invasion ability. However, the mechanism of the up-regulation of GAGE7B needs to be deeply explored. In our previous study, the regulation of GAGE7B by transcription factors was investigated. The core promoter of GAGE7B was firstly identified and the transcription factors potentially bind to the core promoter were predicted. The subsequent results showed that transcription factors YY1 and c-Myc could upregulate GAGE7B expression. c-Myc upregulate GAGE7B expression by binding to the promoter of GAGE7B directly, however, GAGE7B promoter could not be bound by YY1. Intriguingly, the promoter of c-Myc harbor the potential binding site of YY1, which indicated that YY1 might regulate GAGE7B expression in a c-Myc depended manner. Importantly, the mechanism of the regulation of GAGE7B by YY1 will be explored deeply in this study. In addition, the regulation of the progression of gastric cancer by YY1 via regulating c-Myc mediated GAGE7B high expression will be investigated. The study will shed new light on the mechanism of the abnormal expression and function of GAGE7B in gastric cancer.