DNA Methylation-Regulated FAM107A Affects Colorectal Carcinogenesis by Inhibiting FOXM1.

IF 2.7 4区 医学 Q2 SURGERY
Journal of Investigative Surgery Pub Date : 2026-12-01 Epub Date: 2026-03-18 DOI:10.1080/08941939.2026.2633933
Yue Liu, Jinwei Sun, Yuhua Shi, Lisheng Wang, Xinyue Zhang, Lizhou Chen
{"title":"DNA Methylation-Regulated FAM107A Affects Colorectal Carcinogenesis by Inhibiting FOXM1.","authors":"Yue Liu, Jinwei Sun, Yuhua Shi, Lisheng Wang, Xinyue Zhang, Lizhou Chen","doi":"10.1080/08941939.2026.2633933","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Family with sequence similarity 107 member A (FAM107A) has been reported to inhibit cancer cell proliferation and migration and enhance apoptosis; however, to our knowledge, the association between FAM107A and colorectal cancer (CRC) has not been explored.</p><p><strong>Methods: </strong>CCK-8 assay, colony formation, EdU, flow cytometry assays were used to detect the cellular aggressive behaviors. FAM107A promoter methylation was analyzed by bioinformatics tools. The interaction between DNMT1 and FAM107A was explored by RT-qPCR, Western blot and ChIP assay.</p><p><strong>Results: </strong>Overexpression of FAM107A inhibited CRC cell proliferation (<i>p</i> < .001). Furthermore, FAM107A overexpression induced apoptosis (<i>p</i> < .001) and cycle arrest in CRC cells. The direct binding of DNMT1 with FAM107A promoter was demonstrated and DNMT1 silencing enhanced FAM107A expression (<i>p</i> < .001). In addition, FOXM1 overexpression stimulated cell proliferation (<i>p</i> < .05, <i>p</i> < .001) while suppressing cell apoptosis (<i>p</i> < .01) <i>in vitro</i>, and promoted tumor growth (<i>p</i> < .01, <i>p</i> < .001) in a Caco-2 cell subcutaneous nude model <i>in vivo</i>, which was reversed by FAM107A up-regulation (<i>p</i> < .05, <i>p</i> < .01, <i>p</i> < .001).</p><p><strong>Discussion: </strong>These results hypothesize that the occurrence and development of CRC are mainly mediated by the DNMT1/FAM107A/FOXM1 axis.</p>","PeriodicalId":16200,"journal":{"name":"Journal of Investigative Surgery","volume":"39 1","pages":"2633933"},"PeriodicalIF":2.7000,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Investigative Surgery","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/08941939.2026.2633933","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/3/18 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"SURGERY","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction: Family with sequence similarity 107 member A (FAM107A) has been reported to inhibit cancer cell proliferation and migration and enhance apoptosis; however, to our knowledge, the association between FAM107A and colorectal cancer (CRC) has not been explored.

Methods: CCK-8 assay, colony formation, EdU, flow cytometry assays were used to detect the cellular aggressive behaviors. FAM107A promoter methylation was analyzed by bioinformatics tools. The interaction between DNMT1 and FAM107A was explored by RT-qPCR, Western blot and ChIP assay.

Results: Overexpression of FAM107A inhibited CRC cell proliferation (p < .001). Furthermore, FAM107A overexpression induced apoptosis (p < .001) and cycle arrest in CRC cells. The direct binding of DNMT1 with FAM107A promoter was demonstrated and DNMT1 silencing enhanced FAM107A expression (p < .001). In addition, FOXM1 overexpression stimulated cell proliferation (p < .05, p < .001) while suppressing cell apoptosis (p < .01) in vitro, and promoted tumor growth (p < .01, p < .001) in a Caco-2 cell subcutaneous nude model in vivo, which was reversed by FAM107A up-regulation (p < .05, p < .01, p < .001).

Discussion: These results hypothesize that the occurrence and development of CRC are mainly mediated by the DNMT1/FAM107A/FOXM1 axis.

DNA甲基化调控的FAM107A通过抑制FOXM1影响结直肠癌的发生。
简介:序列相似的家族107成员A (FAM107A)被报道抑制癌细胞的增殖和迁移,促进细胞凋亡;然而,据我们所知,FAM107A与结直肠癌(CRC)之间的关系尚未探讨。方法:采用CCK-8法、菌落形成法、EdU、流式细胞术检测细胞侵袭行为。利用生物信息学工具分析FAM107A启动子甲基化。采用RT-qPCR、Western blot和ChIP检测DNMT1与FAM107A的相互作用。结果:FAM107A过表达在体外抑制CRC细胞增殖(p p p p p p p p),在体内促进肿瘤生长(p p p,这一作用被FAM107A上调(p p p)逆转。讨论:这些结果假设CRC的发生发展主要由DNMT1/FAM107A/FOXM1轴介导。
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
CiteScore
4.20
自引率
0.00%
发文量
114
审稿时长
6-12 weeks
期刊介绍: Journal of Investigative Surgery publishes peer-reviewed scientific articles for the advancement of surgery, to the ultimate benefit of patient care and rehabilitation. It is the only journal that encompasses the individual and collaborative efforts of scientists in human and veterinary medicine, dentistry, basic and applied sciences, engineering, and law and ethics. The journal is dedicated to the publication of outstanding articles of interest to the surgical research community.
×
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