UBE2J2-mediated ubiquitination modification of MCM6 regulates proliferation and migration of cervical cancer cells.

IF 3.1 3区 医学 Q2 ONCOLOGY
American journal of cancer research Pub Date : 2026-06-15 eCollection Date: 2026-01-01 DOI:10.62347/SHIF8882
Yanfeng Guo, Yan Zhang, Shuai Zhang, Jingyu Guo, Libing Huang, Zixi Wang, Jiateng Zhong, Hongyan Zhou
{"title":"UBE2J2-mediated ubiquitination modification of MCM6 regulates proliferation and migration of cervical cancer cells.","authors":"Yanfeng Guo, Yan Zhang, Shuai Zhang, Jingyu Guo, Libing Huang, Zixi Wang, Jiateng Zhong, Hongyan Zhou","doi":"10.62347/SHIF8882","DOIUrl":null,"url":null,"abstract":"<p><p>Microchromosome maintenance protein 6 (MCM6), a member of the MCM family, is involved in the regulation of various cancer progression. However, the role and related regulatory mechanisms in cervical cancer are unclear. The aim of this study was to investigate the role of MCM6 in cervical cancer and the regulation of MCM6 protein homeostasis by the ubiquitin-conjugating enzyme E2J2 (UBE2J2). To investigate the expression and function of MCM6 in cervical cancer, we used RT-qPCR and Western blot and found that MCM6 was upregulated. Cell function experiments indicate that MCM6 promotes the proliferation and migration of cervical cancer cells. The GEPIA database identified co-expressed genes with MCM6, and KEGG enrichment analysis showed that MCM6 was significantly associated with UBE2J2. We performed molecular docking of proteins and identified amino acid residues involved in the MCM6-UBE2J2 interaction. Using co-immunoprecipitation and Immunofluorescence experiments, we found that MCM6 binds to UBE2J2 and localizes to the nucleus. Ubiquitination experiments demonstrated that UBE2J2 mediates MCM6 ubiquitination. Response experiments showing that UBE2J2-mediated MCM6 ubiquitination modification regulates the proliferation and migration of cervical cancer cells. Our results suggest that the UBE2J2-MCM6 axis plays an important role in regulating cervical cancer proliferation and migration and is a promising therapeutic target for its treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 6","pages":"2355-2366"},"PeriodicalIF":3.1000,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13373554/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/SHIF8882","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Microchromosome maintenance protein 6 (MCM6), a member of the MCM family, is involved in the regulation of various cancer progression. However, the role and related regulatory mechanisms in cervical cancer are unclear. The aim of this study was to investigate the role of MCM6 in cervical cancer and the regulation of MCM6 protein homeostasis by the ubiquitin-conjugating enzyme E2J2 (UBE2J2). To investigate the expression and function of MCM6 in cervical cancer, we used RT-qPCR and Western blot and found that MCM6 was upregulated. Cell function experiments indicate that MCM6 promotes the proliferation and migration of cervical cancer cells. The GEPIA database identified co-expressed genes with MCM6, and KEGG enrichment analysis showed that MCM6 was significantly associated with UBE2J2. We performed molecular docking of proteins and identified amino acid residues involved in the MCM6-UBE2J2 interaction. Using co-immunoprecipitation and Immunofluorescence experiments, we found that MCM6 binds to UBE2J2 and localizes to the nucleus. Ubiquitination experiments demonstrated that UBE2J2 mediates MCM6 ubiquitination. Response experiments showing that UBE2J2-mediated MCM6 ubiquitination modification regulates the proliferation and migration of cervical cancer cells. Our results suggest that the UBE2J2-MCM6 axis plays an important role in regulating cervical cancer proliferation and migration and is a promising therapeutic target for its treatment.

ube2j2介导的MCM6泛素化修饰调控宫颈癌细胞的增殖和迁移。
微染色体维持蛋白6 (MCM6)是MCM家族的一员,参与多种癌症进展的调控。然而,在子宫颈癌中的作用和相关的调控机制尚不清楚。本研究旨在探讨MCM6在宫颈癌中的作用以及泛素偶联酶E2J2 (UBE2J2)对MCM6蛋白稳态的调节。为了研究MCM6在宫颈癌中的表达和功能,我们采用RT-qPCR和Western blot检测发现MCM6表达上调。细胞功能实验表明,MCM6可促进宫颈癌细胞的增殖和迁移。GEPIA数据库鉴定出与MCM6共表达的基因,KEGG富集分析显示MCM6与UBE2J2显著相关。我们进行了蛋白质的分子对接,并鉴定了参与MCM6-UBE2J2相互作用的氨基酸残基。通过免疫共沉淀和免疫荧光实验,我们发现MCM6与UBE2J2结合并定位到细胞核。泛素化实验证实UBE2J2介导MCM6泛素化。响应实验表明,ube2j2介导的MCM6泛素化修饰可调节宫颈癌细胞的增殖和迁移。我们的研究结果表明,UBE2J2-MCM6轴在调节宫颈癌的增殖和迁移中起重要作用,是一个有希望的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
3.80%
发文量
263
期刊介绍: The American Journal of Cancer Research (AJCR) (ISSN 2156-6976), is an independent open access, online only journal to facilitate rapid dissemination of novel discoveries in basic science and treatment of cancer. It was founded by a group of scientists for cancer research and clinical academic oncologists from around the world, who are devoted to the promotion and advancement of our understanding of the cancer and its treatment. The scope of AJCR is intended to encompass that of multi-disciplinary researchers from any scientific discipline where the primary focus of the research is to increase and integrate knowledge about etiology and molecular mechanisms of carcinogenesis with the ultimate aim of advancing the cure and prevention of this increasingly devastating disease. To achieve these aims AJCR will publish review articles, original articles and new techniques in cancer research and therapy. It will also publish hypothesis, case reports and letter to the editor. Unlike most other open access online journals, AJCR will keep most of the traditional features of paper print that we are all familiar with, such as continuous volume, issue numbers, as well as continuous page numbers to retain our comfortable familiarity towards an academic journal.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书