GXYLT2 serves as a prognostic biomarker and is associated with b-catenin activation and gastric cancer aggressiveness
文献类型：期刊论文
| 作者 | Yang, Jiale2,3; Wu, Jiajun4; Chen, Ziqiang2,3; Hou, Xiangyun2,3; Li, Xiaojing2,3; Liu, Zhaorui5; Yin, Kai5; Pang, Tao5; Huang, Ruimin2,3; Yan, Jun1 |
| 刊名 | GENES & DISEASES
 |
| 出版日期 | 2026-03-01 |
| 卷号 | 13期号:2页码:16 |
| 关键词 | Gastric cancer GXYLT2 Prognostic biomarker Tumor aggressiveness Wnt/beta-catenin signaling |
| ISSN号 | 2352-4820 |
| DOI | 10.1016/j.gendis.2025.101673 |
| 通讯作者 | Pang, Tao(pangtao7667@163.com) ; Huang, Ruimin(rmhuang@simm.ac.cn) ; Yan, Jun(yan_jun@fudan.edu.cn) |
| 英文摘要 | Gastric cancer (GC) is a significant global health challenge due to its high incidence and mortality rate. However, the existing classification methods for GC still have limitations. Given the pivotal role of aberrant glycosylation in GC progression, there is a compelling need to develop a novel molecular classification for this disease. Using a comprehensive analysis of 186 glycogenes across seven public datasets encompassing 1547 GC patients, a 12-glycogene signature-based molecular classification was established, which was linked to tumor stage and prognosis. Among them, the overexpression of glucoside xylosyltransferase 2 (GXYLT2) was positively associated with tumor stage, diffuse subtype, and unfavorable survival outcomes in GC patients. Furthermore, GXYLT2 depletion significantly inhibited the proliferation, invasion, and sphere formation capacities in HGC-27, MKN1, and MKN45 GC cells with diffuse-subtype features, whereas its ectopic expression in AGS and MKN74 GC cells with intestinal subtype did not enhance their aggressive properties. Moreover, RNA sequencing analysis revealed that GXYLT2 knockdown resulted in the decrease of Wnt/b-catenin signaling, which was corroborated by TOPFlash reporter activity, b-catenin phosphorylation, immunofluorescence staining, and nuclear-cytoplasmic separation assays for its nuclear location, via the activation of PP2A complex dependent on GXYLT2-PP2A Aa interaction. Notably, GXYLT2 knockdown significantly suppressed tumorigenicity in vivo. Taken together, we identified GXYLT2 as a potential prognostic biomarker for GC patients, and targeting GXYLT2 suppressed the tumor aggressiveness and inhibited the Wnt/b-catenin pathway, which may provide a potential therapeutic target for GC patients. |
| WOS关键词 | IDENTIFICATION ; SUBTYPES ; DIFFUSE ; CLASSIFICATION ; EXPRESSION ; CARCINOMA ; STOMACH |
| 资助项目 | National Natural Science Foundation of China[82172001] ; Shanghai Municipal Science and Technology Major Project (China) ; Navy Medical University Foundation (China)[2021MS07] |
| WOS研究方向 | Biochemistry & Molecular Biology ; Genetics & Heredity |
| 语种 | 英语 |
| WOS记录号 | WOS:001643867400001 |
| 出版者 | KEAI PUBLISHING LTD |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/322423]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Pang, Tao; Huang, Ruimin; Yan, Jun |
| 作者单位 | 1.Fudan Univ, Lab Anim Ctr, 130 Dongan Rd, Shanghai 200032, Peoples R China 2.Chinese Acad Sci, Shanghai Inst Mat Med, Ctr Drug Safety Evaluat & Res, 555 Zuchongzhi Rd, Shanghai 201203, Peoples R China 3.Univ Chinese Acad Sci, Beijing 100049, Peoples R China 4.Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai 200438, Peoples R China 5.Naval Med Univ, Dept Gastrointestinal Surg, Affiliated Hosp 1, 168 Changhai Rd, Shanghai 200433, Peoples R China |
| 推荐引用方式 GB/T 7714 | Yang, Jiale,Wu, Jiajun,Chen, Ziqiang,et al. GXYLT2 serves as a prognostic biomarker and is associated with b-catenin activation and gastric cancer aggressiveness[J]. GENES & DISEASES,2026,13(2):16. |
| APA | Yang, Jiale.,Wu, Jiajun.,Chen, Ziqiang.,Hou, Xiangyun.,Li, Xiaojing.,...&Yan, Jun.(2026).GXYLT2 serves as a prognostic biomarker and is associated with b-catenin activation and gastric cancer aggressiveness.GENES & DISEASES,13(2),16. |
| MLA | Yang, Jiale,et al."GXYLT2 serves as a prognostic biomarker and is associated with b-catenin activation and gastric cancer aggressiveness".GENES & DISEASES 13.2(2026):16. |
入库方式： OAI收割
来源：上海药物研究所
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