CD36调控DEK与USF1互作介导胃癌迁移侵袭的作用机制

脂代谢相关分子异常与胃癌迁移侵袭的生物学特性相关，但机制不清。前期研究发现脂肪酸受体CD36在胃癌组织和细胞中高表达，促进迁移侵袭，是胃癌预后不良因素；DEK与CD36表达正相关，且能够与USF1结合调控MUC1的表达，促进胃癌细胞迁移侵袭。通过系列前期工作推测，CD36可能通过c-myc正性调控DEK的转录；进一步DEK通过与USF1蛋白互作，促进转录因子USF1正性调控MUC1的转录，进而促进胃癌细胞的迁移侵袭。本项目拟在明确CD36在胃癌组织和细胞内源性表达的基础上，研究CD36通过调控DEK表达；DEK与USF1蛋白互作调控USF1表达; USF1促进MUC1转录，进而促进胃癌迁移侵袭的作用机制；建立裸鼠移植瘤模型验证上述机制；并利用胃癌组织标本，明确CD36、DEK、USF1及MUC1表达与临床病理学参数的相关性。研究旨在阐明CD36促进胃癌迁移侵袭的机制，为胃癌的诊治提供新策略

Lipid metabolism-related molecular abnormalities are associated with the biological characteristics of migration and invasion in gastric cancer, but the mechanism is unclear. Previous studies have found that fatty acid receptor CD36 is highly expressed in gastric cancer tissues and cells, promoting migration and invasion, and is a poor prognosis of gastric cancer. DEK is positively correlated with CD36 expression, and can bind to USF1 to regulate the expression of MUC1 and promote the migration and invasion of gastric cancer cells. Through pre-stage work, it is speculated that CD36 may positively regulate the transcription of DEK through c-myc; further DEK promotes the transcription of USF1 positively regulating MUC1 transcription by interacting with USF1 protein, thereby promoting the migration and invasion of gastric cancer cells. Based on the definition of CD36 in gastric cancer tissues and endogenous expression, CD36 is used to regulate the expression of DEK; DEK and USF1 interact with USF1; USF1 promotes MUC1 transcription, and promotes the migration and invasion of gastric cancer; The nude mouse xenograft model was used to verify the above mechanism; and the correlation between CD36, DEK, USF1 and MUC1 expression and clinicopathological parameters was determined by using gastric cancer tissue samples. The aim of the study was to elucidate the mechanism by which CD36 promotes migration and invasion of gastric cancer, and provides a new strategy for the diagnosis and treatment of gastric cancer.