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幽门螺杆菌感染诱导STAT3/MYBL2/NF-κB轴以促进胃癌进展。

Helicobacter pylori infection induces STAT3/MYBL2/NF-κB axis to promote gastric cancer progression.

作者信息

Feng Zhaotian, Bao Shuqing, Zhu Wenshuai, Xing Yuanxin, Luan Muhua, Ma Xiaoli, Wang Yunshan, Zhu Jingyu, Jia Yanfei

机构信息

Research Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical University, Jinan 250013, PR China; Department of Medical Laboratory, Shandong Second Medical University, Weifang 261053, PR China.

Research Center of Basic Medicine, Central Hospital Affiliated to Shandong First Medical University, Jinan 250013, PR China; Department of Clinical Laboratory, Anqing First People's Hospital of Anhui Medical University, Anqing 246000, PR China.

出版信息

Tissue Cell. 2025 Jun 14;96:103016. doi: 10.1016/j.tice.2025.103016.

DOI:10.1016/j.tice.2025.103016
PMID:40554138
Abstract

Infection with Helicobacter pylori (H. pylori) represents a significant risk factor for the development of gastric cancer (GC). The oncogenic functions of MYBL2 have been reported in several malignancies, for which little research has focused on its effect on H. pylori-induced GC progression. We analyzed the expression and clinical relevance of MYBL2 in GC. H. pylori infection was induced in vitro and in vivo. The effects of MYBL2 on cellular functions were assessed, and tumor growth was evaluated in nude mice injected with genetically altered GC cells. We found H. pylori infection significantly increased MYBL2 expression. Downregulation of MYBL2 inhibited H. pylori-induced cell proliferation and migration. MYBL2 contributed to the growth of subcutaneous xenograft tumors. In conclusion, H. pylori infection upregulated MYBL2 expression by activating STAT3, and MYBL2 was found to be an upstream regulator of NF-κB activation in GC cells. In conclusion, our findings indicate that the H. pylori/STAT3/MYBL2/NF-κB axis plays a critical role in the regulation of GC.

摘要

幽门螺杆菌(H. pylori)感染是胃癌(GC)发生的一个重要危险因素。MYBL2的致癌功能已在多种恶性肿瘤中被报道,但很少有研究关注其对幽门螺杆菌诱导的胃癌进展的影响。我们分析了MYBL2在胃癌中的表达及其临床相关性。在体外和体内诱导幽门螺杆菌感染。评估了MYBL2对细胞功能的影响,并在注射了基因改变的胃癌细胞的裸鼠中评估了肿瘤生长情况。我们发现幽门螺杆菌感染显著增加了MYBL2的表达。MYBL2的下调抑制了幽门螺杆菌诱导的细胞增殖和迁移。MYBL2促进了皮下异种移植肿瘤的生长。总之,幽门螺杆菌感染通过激活STAT3上调MYBL2表达,并且发现MYBL2是胃癌细胞中NF-κB激活的上游调节因子。总之,我们的研究结果表明,幽门螺杆菌/STAT3/MYBL2/NF-κB轴在胃癌的调控中起关键作用。

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