胃癌是目前全球第三致死性的恶性肿瘤，肿瘤侵袭和转移是导致胃癌患者不良预后的主要原因之一。而肿瘤微环境的形成往往促进肿瘤获得侵袭和转移的潜能。RACK1 是一种高度保守的构架蛋白，在信号传导和肿瘤发生发展过程中发挥重要的调控作用。以往针对RACK1的研究一般集中在其对肿瘤细胞自身行为学的影响，而对肿瘤微环境的调节功能尚无报导。在本项目中，我们首次对胃癌细胞中RACK1的表达变化对肿瘤微环境形成和腹膜转移的调控进行研究。我们拟探讨RACK1在胃癌中的表达与肿瘤微环境以及腹膜转移的关系，同时探讨RACK1通过调控CXCL8旁分泌影响肿瘤微环境的功能和分子机制，并在此基础上研究肿瘤微环境在RACK1/CXCL8通路调控胃癌腹膜转移中的作用，以期阐明胃癌细胞通过塑造肿瘤微环境来促进胃癌侵袭转移的新机制，并为胃癌的临床治疗提供新的线索。

Gastric cancer is the third most common cause of cancer-related death worldwide at present, and invasion and metastasis of gastric cancer represent the major reason for its poor prognosis. The formation of tumor microenvironment plays a critical role in stimulating the invasive and metastatic potential of tumor cells. Receptor for activated C-kinase 1 (RACK1) is a highly-conserved scaffold protein, and plays a pivotal role in signal transduction and tumor progression. Previous studies about RACK1 mainly focused on its regulatory effect on tumor behavior itself; however, the role of RACK1 in modulating tumor microenvironment remains little defined. In this study, we examine the effect of RACK1 on tumor microenvironment and peritoneal metastasis in gastric cancer for the first time. We will identify whether altered expression of RACK1 is related to tumor microenvironment formation and peritoneal metastasis of gastric cancer. We will also examine the role of RACK1 in modulating tumor microenvironment through the paracrine of CXCL8, and study the role of tumor microenvironment in stimulating tumor peritoneal metastasis by RACK1/CXCL8 axis, thus elucidating new mechanisms of how gastric cancer cells build tumor microenvironment to stimulate tumor metastasis and providing new clues for the treatment of gastric cancer patients.