HpSlyD是本组率先在本领域报道的一个新的与胃癌变相关的H.pylori毒力因子。近期研究发现，HpSlyD调控TPT1促进肠化生核心因子CDX2及其相关蛋白的表达，但机制不清。通过系列前期工作推测，在HpSlyD上调TPT1促进CDX2表达诱导胃粘膜肠化生表型转变的过程中：HpSlyD可以通过RBPFUS介导的反义长链非编码RNATPT1-AS1转录后调控TPT1的表达；表达增强的TPT1可以促进OCT1的翻译，增加OCT1与CDX2启动子结合，转录激活CDX2表达，最终诱导胃粘膜肠化生表型转变。本研究的目的就是通过体内、外实验验证这一假说，阐明HpSlyD调控胃粘膜肠化生的分子机制。本研究将为H.pylori感染的临床监控及“因型施治”提供重要分子靶点，为阻断H.pylori相关性肠化生形成，进而降低胃癌变发展提供新的思路及策略。

HpslyD is a new virulence factors of H.pylori related to gastric carcinogenesis that has been first reported by our group in this field. Recent studies have found that HpSlyD regulates TPT1 to promote the expression of intestinal metaplastic factor CDX2 and its related proteins, but the mechanism is unclear. Through a series of preliminary work, we propose in the process of HpSlyD up-regulating TPT1 to induce CDX2 expression，HpSlyD can regulate post-transcriptional TPT1 expression by RBP FUS-mediated long non-coding RNA TPT1-AS1; enhancing expressed TPT1 then promote the translation of OCT1, increasing the binding of OCT1 to the promoter of CDX2 and transcriptional activating the expression of CDX2. As a result, it could induce the phenotype transition of gastric intestinal metaplasia. This study aims to validate this hypothesis by in vivo and in vitro experiments, and to elucidate the molecular mechanism by which HpSlyD regulates gastric intestinal metaplasia. This study will provide important molecular targets for the clinical monitoring and "type-based treatment" of H. pylori infection, and provide new ideas and strategies for blocking the formation of H.pylori-related intestinal metaplasia and further reducing the development of gastric cancer.