环状RNA circPTK2/miR-125a/STAT3 途径在幽门螺杆菌介导的胃癌进展中的作用及机制研究

幽门螺杆菌（HP）引起的慢性感染是胃癌发病的主要原因之一，其引起的宿主免疫应答涉及多种炎症反应和致癌信号通路，其中STAT3是各种通路的中心途径，但HP感染对STAT3的触发机制尚不明确。近年研究发现，环状RNA可以通过吸附miRNA参与转录后水平的调控，或可参与到细菌感染引发的肿瘤恶性转变中。项目组前期筛选到了参与胃癌进展及其他炎症反应的circPTK2，生物信息学预测其具有多个miR-125a结合位点，且STAT3是miR-125a调控的下游靶基因。因此，推测circPTK2通过吸附miR-125a调控STAT3的表达促进HP介导的胃癌进展。本项目将基于前期测序结果，使用RNA pull down、RNA FISH、细胞转染等技术，深入探讨CircPTK2/miR-125a/STAT3 途径在HP介导的胃癌进展中的作用机制，为环状RNA在感染所致的肿瘤进展方面的研究

Chronic infection caused by helicobacter pylori (HP) is one of the main causes of gastric cancer. The host immune response caused by HP involves a variety of inflammatory responses and carcinogenic signaling pathways. STAT3 is the central pathway among of them, but the trigger mechanism of HP infection on STAT3 is still unclear. In recent years, circular RNA plays a regulatory role in post-transcriptional levels through the adsorption of microRNA, it may be involved in malignant transformation of tumor caused by bacterial infection. CircPTK2,.which is involved in the progression of gastric cancer and other inflammatory reactions, was screened in the previous study. Bioinformatics predicted that CircPTK2 had multiple mir-125a binding sites, and STAT3 is the direct target regulated by miR-125a. Therefore, it is speculated that circPTK2 promoted HP-induced gastric cancer progression through adsorption of miR-125a, which regulated the expression of STAT3. Based on the previous sequencing results, this project will use RNA pull down, RNA FISH, cell transfection and other technologies to deeply explore the mechanism of the CircPTK2/ mir-125a /STAT3 axis in HP-induced progression of gastric cancer, providing new ideas for circular RNA in the study of tumor progression caused by infection.