胃癌（GC）是消化道常见的致命恶性肿瘤，尤其在亚洲地区。循环RNA（circRNA）已被证明在多种肿瘤中，包括GC，调控恶性进展和免疫治疗效果。值得注意的是，circRNA在GC中的功能尚未完全揭示。因此，探索更多与GC相关的circRNA可能为GC治疗提供潜在策略。在本研究中，观察到hsa_circ_0001479在GC中表达水平较高，并随后发现与浸润深度、淋巴结转移和TNM分期有关。功能上，通过多种实验如CCK-8、EdU、克隆形成和转移等，发现hsa_circ_0001479的过表达增强了GC细胞的增殖和迁移。双荧光酶报告基因实验证明hsa_circ_0001479通过海绵吸附miR-133a-5p上调DEK表达。进一步的研究表明，DEK通过激活Wnt/β-连环蛋白通路促进了β-连环蛋白进入细胞核，从而促进了下游c-Myc的累积。作为转录因子，c-Myc与hsa_circ_0001479母基因的启动子结合，刺激hsa_circ_0001479的生成。此外，hsa_circ_0001479抑制了GC中CD8+T细胞的浸润并与免疫检查点相关。总之，hsa_circ_0001479加速了GC的发展和转移，并介导了CD8+T细胞的免疫逃避。针对其可能为更好地局部治疗GC、降低转移发生率提供了一种新型的免疫治疗方法。版权所有©2023 Elsevier B.V. 保留所有权利。

Gastric cancer (GC) is a common fatal malignant tumor of the digestive tract, particularly in Asia. Circular RNA (circRNA) has been proved to regulate malignancy progression and immunotherapeutic efficacy in multiple tumors, including GC. Notably, the function of circRNAs in GC has not been completely revealed. Therefore, exploration of more GC related circRNAs may provide potential strategies for GC treatment. In the study, it was observed that hsa_circ_0001479 exhibited a high level of expression in GC and was subsequently found to be associated with the depth of invasion, lymph node metastasis, and TNM stage. Functionally, the overexpression of hsa_circ_0001479 was found to enhance the proliferation and migration of GC cells, as evidenced by various experiments such as CCK-8, EdU, colony forming and transwell. Dual-luciferase reporter assay verified that hsa_circ_0001479 upregulated DEK expression by sponge targeting miR-133a-5p. Further investigations indicated DEK affected the entry of β-catenin into the nucleus by activating Wnt/β-catenin signaling pathway to promote accumulation of downstream c-Myc. As a transcription factor, c-Myc combined with the promoter of hsa_circ_0001479 parent gene to stimulate hsa_circ_0001479 generation. Besides, hsa_circ_0001479 inhibited theinfiltration with CD8+T cells in GC and associated with immune checkpoints. In summary, hsa_circ_0001479 accelerated the development and metastasis of GC and mediates immune escape of CD8+T cells. Targeting it may provide a novel immunotherapy to better locally treat GC and reduce the incidence of metastases.Copyright © 2023 Elsevier B.V. All rights reserved.