文献类型：期刊文献

英文题名：COPB2 drives gastric cancer progression via PI3K/AKT/NF-κB signaling: a multi-omics and functional study

作者：Li, Hailong[1,2,3];Wei, Dong[4];Gao, Xiaqing[3];Su, Rong[3];Yang, Chunting[3];Tang, Ping[5];Yu, Xiqiu[6];Wu, Yuhong[7]

第一作者：Li, Hailong;李海龙

通信作者：Yu, XQ[1];Wu, YH[2]

机构：[1]Shenzhen Integrated Tradit Chinese & Western Med, Dept Geriatr, Shenzhen, Guangdong, Peoples R China;[2]Gansu Prov Hosp, NHC Key Lab Diag & Therapy Gastrointestinal Tumor, Lanzhou, Peoples R China;[3]Gansu Univ Chinese Med, Sch Clin Med 1, Dept Internal Med, Lanzhou, Peoples R China;[4]Luohu Dist Tradit Chinese Med Hosp, Dept Prevent Med, Shenzhen, Peoples R China;[5]Shantou Univ, Luohu Clin Coll, Sch Med, Dept Gen Practice, Shenzhen, Peoples R China;[6]Luohu Dist Peoples Hosp, Dept Gastroenterol, Shenzhen 518000, Peoples R China;[7]Shenzhen Univ, South China Hosp, Hlth Sci Ctr, Dept Chinese Med, 1 Fuxin Rd, Shenzhen 518116, Peoples R China

第一机构：Shenzhen Integrated Tradit Chinese & Western Med, Dept Geriatr, Shenzhen, Guangdong, Peoples R China

通信机构：[1]corresponding author), Luohu Dist Peoples Hosp, Dept Gastroenterol, Shenzhen 518000, Peoples R China;[2]corresponding author), Shenzhen Univ, South China Hosp, Hlth Sci Ctr, Dept Chinese Med, 1 Fuxin Rd, Shenzhen 518116, Peoples R China.

年份：2026

卷号：20

期号：1

外文期刊名：CELL ADHESION & MIGRATION

收录：;Scopus(收录号：2-s2.0-105029004879);WOS:【SCI-EXPANDED(收录号:WOS:001676785800001)】；

基金：This study was supported by the Joint Research Fund of the Provincial Science and Technology Program of Gansu Province [23JRRA1527], the open fund of the Key Laboratory of gastrointestinal tumor diagnosis and treatment of the National Health Commission [NLDTG2020012], the Shenzhen Collaborative Innovation Technology Plan [2022420667], and the Shenzhen Science and Technology Program [JCYJ20250604190013017].

语种：英文

外文关键词：COPB2; gastric cancer; Ingenuity Pathway Analysis; microarray; tissue microarray

摘要：This study investigated the role of COPB2 in gastric cancer (GC) pathogenesis. Analysis of TCGA datasets and tissue microarrays revealed its upregulation in GC tissues compared to normal adjacent tissues, which was correlated with advanced tumor stage and lymphatic invasion and demonstrated significant diagnostic value (AUC = 0.895 and 0.851). Functional assays using lentiviral-mediated silencing in GC cells showed that COPB2 knockdown suppressed cell proliferation and migration, induced G0/G1-phase arrest, and promoted apoptosis. Mechanistic investigations through microarray, KEGG, and IPA analyses indicated that COPB2 dysregulation inactivated the PI3K/AKT and NF-kappa B signaling pathways. This led to the downregulation of key oncogenic effectors including Slug, FN1, CDH2, F2RL1, CDK6, CCND1, MMP9, CDKN2A, and SQSTM1, while upregulating tumor suppressors CDKN1B, CDKN1A, and DDIT3. In conclusion, COPB2 acts as an oncogene in GC, driving tumor progression through modulation of the cell cycle and key signaling pathways, highlighting its potential as a therapeutic target.