本课题以细胞膜表面受体蛋白GPR35为出发点，以癌症线粒体代谢障碍为线索，通过查阅文献和前期工作，首先明确了GPR35在乳腺癌发病时表达显著增高，过表达GPR35激活mTOR信号通路，同时降低miRNA-548a-3p表达。.TRAP1在乳腺癌变过程中高表达，增加线粒体外膜的通透性，抑制细胞色素C释放而引起线粒体损伤。miRNA 可以通过调控mRNA的转录后表达，参与细胞代谢调节，通过前期试验我们发现miRNA-548a-3p可以下调TRAP1的表达，改善线粒体损伤程度。.因此，我们推测GPR35-mTOR- miRNA-548a-3p-TRAP1途径可能是导致乳腺细胞癌细胞线粒体功能损失，诱导细胞癌变的一条重要途径，项目拟对在临床、细胞、动物实验三个层面进行研究，探究GPR35调控mTOR信号通路介导miRNA-548a-3p调节乳腺癌线粒体功能的作用机制，为临床乳腺癌治疗提供理论依据。

In this study, GPR35, a cell membrane surface receptor protein, was used as a starting point and cancer mitochondrial metabolic disorder as a clue. By consulting the literature and previous work, we first identified that GPR35 was significantly increased in breast cancer. Overexpression of GPR35 activated the mTOR signaling pathway and decreased the expression of microRNA-548a-3p..TRAP1 is highly expressed in breast cancer, which increases the permeability of mitochondrial extracorporeal membrane and inhibits the release of cytochrome C, resulting in mitochondrial damage. MicroRNAs can regulate the post-transcriptional expression of RNA and participate in the regulation of cell metabolism. Previous experiments showed that microRNAs-548a-3p can down-regulate the expression of TRAP1 and improve the degree of mitochondrial damage..Therefore, we speculate that GPR35-mTOR-microNA-548a-3p-TRAP1 pathway may be an important pathway leading to the loss of mitochondrial function of breast cancer cells and the induction of cell carcinogenesis. This project aims to study the mechanism of GPR35 regulating mTOR signaling pathway mediating the regulation of microNA-548a-3p on the mitochondrial function of breast cancer cells in clinical, cellular and animal experiments, and to explore the mechanism of GPR35 regulating mTOR signaling pathway mediating the regulation of microNA-548a-3 Cancer treatment provides a theoretical basis.