Zhaotian Feng , Shuqing Bao , Wenshuai Zhu , Yuanxin Xing , Muhua Luan , Xiaoli Ma , Yunshan Wang , Jingyu Zhu , Yanfei Jia
{"title":"幽门螺杆菌感染诱导STAT3/MYBL2/NF-κB轴促进胃癌进展","authors":"Zhaotian Feng , Shuqing Bao , Wenshuai Zhu , Yuanxin Xing , Muhua Luan , Xiaoli Ma , Yunshan Wang , Jingyu Zhu , Yanfei Jia","doi":"10.1016/j.tice.2025.103016","DOIUrl":null,"url":null,"abstract":"<div><div>Infection with <em>Helicobacter pylori</em> (<em>H. pylori</em>) 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 <em>H. pylori</em>-induced GC progression. We analyzed the expression and clinical relevance of MYBL2 in GC. <em>H. pylori</em> 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 <em>H. pylori</em> infection significantly increased MYBL2 expression. Downregulation of MYBL2 inhibited <em>H. pylori</em>-induced cell proliferation and migration. MYBL2 contributed to the growth of subcutaneous xenograft tumors. In conclusion, <em>H. pylori</em> 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 <em>H. pylori</em>/STAT3/MYBL2/NF-κB axis plays a critical role in the regulation of GC.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"96 ","pages":"Article 103016"},"PeriodicalIF":2.7000,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Helicobacter pylori infection induces STAT3/MYBL2/NF-κB axis to promote gastric cancer progression\",\"authors\":\"Zhaotian Feng , Shuqing Bao , Wenshuai Zhu , Yuanxin Xing , Muhua Luan , Xiaoli Ma , Yunshan Wang , Jingyu Zhu , Yanfei Jia\",\"doi\":\"10.1016/j.tice.2025.103016\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Infection with <em>Helicobacter pylori</em> (<em>H. pylori</em>) 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 <em>H. pylori</em>-induced GC progression. We analyzed the expression and clinical relevance of MYBL2 in GC. <em>H. pylori</em> 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 <em>H. pylori</em> infection significantly increased MYBL2 expression. Downregulation of MYBL2 inhibited <em>H. pylori</em>-induced cell proliferation and migration. MYBL2 contributed to the growth of subcutaneous xenograft tumors. In conclusion, <em>H. pylori</em> 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 <em>H. pylori</em>/STAT3/MYBL2/NF-κB axis plays a critical role in the regulation of GC.</div></div>\",\"PeriodicalId\":23201,\"journal\":{\"name\":\"Tissue & cell\",\"volume\":\"96 \",\"pages\":\"Article 103016\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2025-06-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Tissue & cell\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0040816625002964\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ANATOMY & MORPHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue & cell","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0040816625002964","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}
Helicobacter pylori infection induces STAT3/MYBL2/NF-κB axis to promote gastric cancer progression
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.
期刊介绍:
Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed.
Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.