{"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.
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。
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.