Lingyan Jin, Hye-Yeong Jin, Meihui Li, Younghoon Kim, Nam-Yun Cho, Jeong Mo Bae, Gyeong Hoon Kang
{"title":"低甲基化ZNF793在胃癌中的致癌作用:对细胞存活和干细胞的关注","authors":"Lingyan Jin, Hye-Yeong Jin, Meihui Li, Younghoon Kim, Nam-Yun Cho, Jeong Mo Bae, Gyeong Hoon Kang","doi":"10.1007/s10120-025-01632-8","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Although genome-wide promoter CpG island hypermethylation of Epstein-Barr virus-associated gastric carcinoma (EBV GC) is well known, ZNF793 is rarely methylated in EBV GC but is frequently methylated in other molecular subtypes of GC, including microsatellite instability-high GC. Based on the hypothesis that ZNF793 may be important for cell survival and stemness in EBV GC, the oncogenic role of ZNF793 was investigated.</p><p><strong>Methods: </strong>ZNF793 expression was knocked out and then restored in EBV and non-EBV GC cell lines, and its effects on cell proliferation, cell migration, cell invasion, tumor sphere formation, and xenograft tumor formation were assessed.</p><p><strong>Results: </strong>ZNF793 knockout significantly suppressed the migration, invasion, proliferation, and stemness in GC cells with ZNF793 expression. Additionally, ZNF793 knockout significantly inhibited tumor growth in a xenograft tumor model.</p><p><strong>Conclusions: </strong>These results suggest that ZNF793 plays an oncogenic role in not only EBV GC but also other subtypes of GC and may be a potential therapeutic target.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"814-824"},"PeriodicalIF":5.1000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12378280/pdf/","citationCount":"0","resultStr":"{\"title\":\"The oncogenic role of hypomethylated ZNF793 in gastric carcinoma: a focus on cell survival and stemness.\",\"authors\":\"Lingyan Jin, Hye-Yeong Jin, Meihui Li, Younghoon Kim, Nam-Yun Cho, Jeong Mo Bae, Gyeong Hoon Kang\",\"doi\":\"10.1007/s10120-025-01632-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Although genome-wide promoter CpG island hypermethylation of Epstein-Barr virus-associated gastric carcinoma (EBV GC) is well known, ZNF793 is rarely methylated in EBV GC but is frequently methylated in other molecular subtypes of GC, including microsatellite instability-high GC. Based on the hypothesis that ZNF793 may be important for cell survival and stemness in EBV GC, the oncogenic role of ZNF793 was investigated.</p><p><strong>Methods: </strong>ZNF793 expression was knocked out and then restored in EBV and non-EBV GC cell lines, and its effects on cell proliferation, cell migration, cell invasion, tumor sphere formation, and xenograft tumor formation were assessed.</p><p><strong>Results: </strong>ZNF793 knockout significantly suppressed the migration, invasion, proliferation, and stemness in GC cells with ZNF793 expression. Additionally, ZNF793 knockout significantly inhibited tumor growth in a xenograft tumor model.</p><p><strong>Conclusions: </strong>These results suggest that ZNF793 plays an oncogenic role in not only EBV GC but also other subtypes of GC and may be a potential therapeutic target.</p>\",\"PeriodicalId\":12684,\"journal\":{\"name\":\"Gastric Cancer\",\"volume\":\" \",\"pages\":\"814-824\"},\"PeriodicalIF\":5.1000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12378280/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Gastric Cancer\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s10120-025-01632-8\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/6/22 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gastric Cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10120-025-01632-8","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/6/22 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
The oncogenic role of hypomethylated ZNF793 in gastric carcinoma: a focus on cell survival and stemness.
Background: Although genome-wide promoter CpG island hypermethylation of Epstein-Barr virus-associated gastric carcinoma (EBV GC) is well known, ZNF793 is rarely methylated in EBV GC but is frequently methylated in other molecular subtypes of GC, including microsatellite instability-high GC. Based on the hypothesis that ZNF793 may be important for cell survival and stemness in EBV GC, the oncogenic role of ZNF793 was investigated.
Methods: ZNF793 expression was knocked out and then restored in EBV and non-EBV GC cell lines, and its effects on cell proliferation, cell migration, cell invasion, tumor sphere formation, and xenograft tumor formation were assessed.
Results: ZNF793 knockout significantly suppressed the migration, invasion, proliferation, and stemness in GC cells with ZNF793 expression. Additionally, ZNF793 knockout significantly inhibited tumor growth in a xenograft tumor model.
Conclusions: These results suggest that ZNF793 plays an oncogenic role in not only EBV GC but also other subtypes of GC and may be a potential therapeutic target.
期刊介绍:
Gastric Cancer is an esteemed global forum that focuses on various aspects of gastric cancer research, treatment, and biology worldwide.
The journal promotes a diverse range of content, including original articles, case reports, short communications, and technical notes. It also welcomes Letters to the Editor discussing published articles or sharing viewpoints on gastric cancer topics.
Review articles are predominantly sought after by the Editor, ensuring comprehensive coverage of the field.
With a dedicated and knowledgeable editorial team, the journal is committed to providing exceptional support and ensuring high levels of author satisfaction. In fact, over 90% of published authors have expressed their intent to publish again in our esteemed journal.