Epstein-Barr virus nuclear antigen 1 (EBNA1) increases the expression levels of MDM2 and MDM4 genes in HeLa cells: a review on MDM2 and MDM4 roles in cancer.
Seyed Mohammad Ali Hashemi, Amir Hossein Alipour, Sima Emamifar, Ali Farhadi, Jamal Sarvari
{"title":"Epstein-Barr virus nuclear antigen 1 (EBNA1) increases the expression levels of MDM2 and MDM4 genes in HeLa cells: a review on MDM2 and MDM4 roles in cancer.","authors":"Seyed Mohammad Ali Hashemi, Amir Hossein Alipour, Sima Emamifar, Ali Farhadi, Jamal Sarvari","doi":"10.1186/s13104-025-07275-3","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Epstein-Barr virus nuclear antigen 1 (EBNA1) is a key viral protein expressed in all latency phases and EBV-associated tumors. It can modulate the expression of various host and viral genes. This study aimed to investigate the impact of EBNA1 on the expression levels of two cellular genes involved in p53 pathway regulation-MDM2 and MDM4-in HeLa cells. This investigation was conducted as part of our broader research on EBV-related oncogenic mechanisms.</p><p><strong>Results: </strong>HeLa cells were transfected with either an EBNA1-expressing plasmid or a control plasmid. Gene expression levels of MDM2 and MDM4 were analyzed using real-time PCR. The results demonstrated a statistically significant increase in MDM4 expression in EBNA1-transfected cells compared to controls (p = 0.028). Although MDM2 expression was also elevated, the difference was not statistically significant (p = 0.11). These findings suggest that EBNA1 may play a role in cervical cancer development by upregulating genes that inhibit p53 tumor suppressor activity.</p>","PeriodicalId":9234,"journal":{"name":"BMC Research Notes","volume":"18 1","pages":"221"},"PeriodicalIF":1.6000,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12084995/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BMC Research Notes","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1186/s13104-025-07275-3","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Epstein-Barr virus nuclear antigen 1 (EBNA1) is a key viral protein expressed in all latency phases and EBV-associated tumors. It can modulate the expression of various host and viral genes. This study aimed to investigate the impact of EBNA1 on the expression levels of two cellular genes involved in p53 pathway regulation-MDM2 and MDM4-in HeLa cells. This investigation was conducted as part of our broader research on EBV-related oncogenic mechanisms.
Results: HeLa cells were transfected with either an EBNA1-expressing plasmid or a control plasmid. Gene expression levels of MDM2 and MDM4 were analyzed using real-time PCR. The results demonstrated a statistically significant increase in MDM4 expression in EBNA1-transfected cells compared to controls (p = 0.028). Although MDM2 expression was also elevated, the difference was not statistically significant (p = 0.11). These findings suggest that EBNA1 may play a role in cervical cancer development by upregulating genes that inhibit p53 tumor suppressor activity.
BMC Research NotesBiochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
3.60
自引率
0.00%
发文量
363
审稿时长
15 weeks
期刊介绍：
BMC Research Notes publishes scientifically valid research outputs that cannot be considered as full research or methodology articles. We support the research community across all scientific and clinical disciplines by providing an open access forum for sharing data and useful information; this includes, but is not limited to, updates to previous work, additions to established methods, short publications, null results, research proposals and data management plans.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
