溶血磷脂酸受体2（LPAR2，EDG4）是G蛋白偶联受体家族EDG组的成员。目前已证实，LPAR2在各种肿瘤细胞中表达大幅增加，在肿瘤细胞生存与转移中起重要作用，我们发现，LPA通过LPAR2信号通路诱导胃癌细胞CD147表达增加。这意味着细胞迁移活性得以增强，CD147是作为基质金属蛋白酶诱导物参与细胞迁移；又对乳酸转运体活性所必需的与其共表达的分子伴侣。可推断，使肿瘤细胞防止酸中毒性死亡很可能是LPA/LPAR2抗凋亡的一种新机制。.该课题在前期基础上，首先弄清LPA/LPAR2诱导CD147的详细信号通路；重点阐明G偶联蛋白的类型、MAP激酶类型、第二信使、转录因子的参与；考察LPA/LPAR2通路与EGF受体及其通路之间、与乳酸转运体表达量及其活性之间和与LPA抗凋亡作用之间关系。研究结果将对肿瘤的发生、发展过程及其治疗小分子靶位点的探究方面，均提供有价值的理论依据。

Lysophosphotidic acid receptor 2 (LPAR2, EDG4) is EDG member of G protein coupled receptor family.The present study has proved that LPAR2 expression greatly increased in many tumor cells, and play an important role in tumor cell survival and transfer.We found that LPA induces CD147 production was mediated by LPAR2 signaling pathway in gastric cancer cells. CD147 stimulates the cells migration through activating matrix metalloproteinases,In addition,CD147 and MCT is a pair of co-expressing chaperone and CD147 is required for MCT activity，so，it'll be deduced that LPA/LPAR2 may contribute to protect the tumor cells from apoptosis caused by acidosis，indicating a new mechanism for antiapoptotic action of LPA/LPAR2..In this study ，we try to clarify the detailed signaling pathway involved in CD147 induction by LPA through LPAR2,focusing on the G coupling protein, MAP kinases, second messengers, related transcription factors. To investigate the relationship between LPA/LPAR2 signaling and EGF receptors, involvement of lactate transporter expression and LPA antiapoptotic action. Our results may be to provide a valuable theoretical basis for tumor occurrence,development and the small molecules targeted treatment.