Zihua Zhou, Siyi Liu, Chenyu Zhang, Jun Deng, Lin Liang, Yanhong Zhou
{"title":"CD90 Promotes Gastric Cancer Progression by Regulating SLC1A5-Mediated Glutamine Metabolism Through YY1","authors":"Zihua Zhou, Siyi Liu, Chenyu Zhang, Jun Deng, Lin Liang, Yanhong Zhou","doi":"10.1111/cas.70377","DOIUrl":null,"url":null,"abstract":"<p>CD90 (THY1) is a cell surface glycoprotein that plays a crucial role in the occurrence and development of various malignant tumors. It affects tumor cell proliferation, metastasis, angiogenesis, stem cell characteristics, and energy metabolism. CD90 is an important biomarker for many malignant tumors and is closely related to tumor prognosis. However, the role and specific mechanisms of CD90 in glutamine metabolism in gastric cancer (GC) cells remain incompletely understood. In this study, we report that CD90 affects glutamine metabolism in GC cells through SLC1A5, ultimately promoting GC progression. Mechanistically, CD90 promotes the binding of YY1 to the SLC1A5 promoter, enhances the transcriptional activity of the SLC1A5 promoter, and increases its transcriptional level. This, in turn, affects SLC1A5-mediated glutamine metabolism and ferroptosis in GC cells, ultimately facilitating GC progression. Our results suggest that CD90 plays an important role in regulating glutamine metabolism in GC cells, providing important experimental evidence for elucidating the pathogenesis of GC.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 6","pages":"1748-1765"},"PeriodicalIF":4.9000,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70377","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Science","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/cas.70377","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/3/31 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
CD90 (THY1) is a cell surface glycoprotein that plays a crucial role in the occurrence and development of various malignant tumors. It affects tumor cell proliferation, metastasis, angiogenesis, stem cell characteristics, and energy metabolism. CD90 is an important biomarker for many malignant tumors and is closely related to tumor prognosis. However, the role and specific mechanisms of CD90 in glutamine metabolism in gastric cancer (GC) cells remain incompletely understood. In this study, we report that CD90 affects glutamine metabolism in GC cells through SLC1A5, ultimately promoting GC progression. Mechanistically, CD90 promotes the binding of YY1 to the SLC1A5 promoter, enhances the transcriptional activity of the SLC1A5 promoter, and increases its transcriptional level. This, in turn, affects SLC1A5-mediated glutamine metabolism and ferroptosis in GC cells, ultimately facilitating GC progression. Our results suggest that CD90 plays an important role in regulating glutamine metabolism in GC cells, providing important experimental evidence for elucidating the pathogenesis of GC.
期刊介绍:
Cancer Science (formerly Japanese Journal of Cancer Research) is a monthly publication of the Japanese Cancer Association. First published in 1907, the Journal continues to publish original articles, editorials, and letters to the editor, describing original research in the fields of basic, translational and clinical cancer research. The Journal also accepts reports and case reports.
Cancer Science aims to present highly significant and timely findings that have a significant clinical impact on oncologists or that may alter the disease concept of a tumor. The Journal will not publish case reports that describe a rare tumor or condition without new findings to be added to previous reports; combination of different tumors without new suggestive findings for oncological research; remarkable effect of already known treatments without suggestive data to explain the exceptional result. Review articles may also be published.