文献类型：期刊文献

英文题名：SYT15B promotes tumor progression through interaction with IQGAP1 to activate the MAPK pathway in lung adenocarcinoma

作者：Ren, Yue[1,2];Li, Tianyi[1,2];Zhou, Heng[1,3];Cui, Yuqing[2];Li, Chenghao[1,4];Shen, Weigan[1];Sun, Haibo[1];Mao, Haiyan[2];Zhang, Zhengrong[2];Wang, Zheng[5];Ling, Zhi[1,2];Chen, Yong[1,2];Yin, Xudong[1,2]

第一作者：Ren, Yue

通信作者：Chen, Y[1];Yin, XD[1]

机构：[1]Yangzhou Univ, Med Coll, Yangzhou, Peoples R China;[2]Yangzhou Univ, Dept Oncol, Affiliated Hosp, Yangzhou, Peoples R China;[3]Yangzhou Univ, Sch Publ Hlth, Yangzhou, Peoples R China;[4]Gansu Univ Chinese Med, Clin Coll Chinese Med, Lanzhou, Peoples R China;[5]Yangzhou Univ, Affiliated Hosp, Dept Pathol, Yangzhou, Peoples R China

第一机构：Yangzhou Univ, Med Coll, Yangzhou, Peoples R China

通信机构：[1]corresponding author), Yangzhou Univ, Med Coll, Yangzhou, Peoples R China.

年份：2026

卷号：139

外文期刊名：CELLULAR SIGNALLING

收录：;Scopus(收录号：2-s2.0-105024216120);WOS:【SCI-EXPANDED(收录号:WOS:001640096100001)】；

基金：The research was supported by the Postgraduate Research & Practice Innovation Program of Jiangsu Province (Project no. SJCX22-1818) , National Natural Science Foundation of China (grant no. BK20251845) , Yangzhou Social Development project (Project no. YZ2024077) , Yangzhou University's Special Fund for Medical Innovation and Translational Medicine (Project no. AHYZUCXTD202102) and the Project from Yangzhou key discipline in oncology therapeutics (Project YZYXZDXK-013) .

语种：英文

外文关键词：SYT15B; IQGAP1; MAPK; Lung adenocarcinoma; Calcium signalling

摘要：Lung adenocarcinoma (LUAD) the predominant subtype of lung cancer, is characterized by rapid tumor growth, local invasion, and distant metastasis. Since dysregulated expression of synaptotagmin (SYT) proteins have been implicated in the development and progression of LUAD, the specific role and mechanisms of SYT15B in LUAD remain unclear. This study demonstrates that elevated SYT15B expression drives malignant progression and predicts poor prognosis in LUAD, as evidenced by integrated clinical sample, in vitro, and in vivo analyses. We identify a novel molecular mechanism whereby SYT15B interacts with IQ motif-containing GTPase-activating protein 1 (IQGAP1), leading to activation of the MAPK signalling pathway and subsequent promotion of aggressive tumor phenotypes. Disruption of the SYT15B-IQGAP1 interaction through IQGAP1 knockdown attenuated MAPK signalling pathway activation and reversed the oncogenic phenotype induced by SYT15B. Notably, specific inhibition of intracellular calcium with BAPTA can also attenuates SYT15B-IQGAP1 complex formation, abrogates MAPK signalling activation, and reverses SYT15B-mediated oncogenic effects. These findings establish the calcium-dependent SYT15B/IQGAP1/MAPK axis as a potential therapeutic and prognostic biomarker in LUAD.