m6A甲基化调节剂rbm15介导的ITGBL1 mRNA稳定性上调通过重塑肿瘤微环境加重结肠癌进展

IF 1.4 4区 医学 Q4 GASTROENTEROLOGY & HEPATOLOGY Turkish Journal of Gastroenterology Pub Date : 2025-01-13 DOI:10.5152/tjg.2025.24068
Jie Zhu, Dengliang Liu, Yingying Zou
{"title":"m6A甲基化调节剂rbm15介导的ITGBL1 mRNA稳定性上调通过重塑肿瘤微环境加重结肠癌进展","authors":"Jie Zhu, Dengliang Liu, Yingying Zou","doi":"10.5152/tjg.2025.24068","DOIUrl":null,"url":null,"abstract":"<p><strong>Background/aims: </strong>Colon adenocarcinoma (COAD) is a prevalent malignant tumor of the digestive system. Previous research has indicated that RNA N6-methyladenosine (m6A) methyltransferase RNA-binding motif protein-15 (RBM15) is involved in various cancers. We aimed to investigate the function of RBM15 in COAD progression and its underlying molecular mechanism.</p><p><strong>Materials and methods: </strong>TIMER and UALCAN databases were applied to analyze the relationship between COAD and Integrin β-like 1 protein (ITGBL1) or RBM15. RT-qPCR and Western blot were used to analyze ITGBL1, M2-type macrophage markers, EMT-related markers, and RBM15 expression. CCK-8, colony formation, and transwell experiments detected cell viability, proliferation, migration, and invasion. The effect of ITGBL1 on COAD tumor growth was examined using a xenograft tumor model. The effects of COAD cells on macrophage polarization and the proliferation and apoptosis of CD8+ T cells were analyzed using flow cytometry analysis. Relationships between RBM15 and ITGBL1 were validated using MeRIP and dual-luciferase reporter assay.</p><p><strong>Results: </strong>ITGBL1 and RBM15 contents were elevated in COAD. ITGBL1 knockdown could hinder COAD cell proliferation, migration, invasion, M2-type macrophage polarization, and lymphocyte immunity. Meanwhile, the lack of RBM15 dampened tumor growth in vivo. Mechanistically, RBM15 could increase ITGBL1 expression by m6A methylation.</p><p><strong>Conclusion: </strong>RBM15 could promote COAD progression by regulating ITGBL1 mRNA stability, providing a promising biomarker and a potential target for COAD.</p>","PeriodicalId":51205,"journal":{"name":"Turkish Journal of Gastroenterology","volume":" ","pages":""},"PeriodicalIF":1.4000,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment.\",\"authors\":\"Jie Zhu, Dengliang Liu, Yingying Zou\",\"doi\":\"10.5152/tjg.2025.24068\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background/aims: </strong>Colon adenocarcinoma (COAD) is a prevalent malignant tumor of the digestive system. Previous research has indicated that RNA N6-methyladenosine (m6A) methyltransferase RNA-binding motif protein-15 (RBM15) is involved in various cancers. We aimed to investigate the function of RBM15 in COAD progression and its underlying molecular mechanism.</p><p><strong>Materials and methods: </strong>TIMER and UALCAN databases were applied to analyze the relationship between COAD and Integrin β-like 1 protein (ITGBL1) or RBM15. RT-qPCR and Western blot were used to analyze ITGBL1, M2-type macrophage markers, EMT-related markers, and RBM15 expression. CCK-8, colony formation, and transwell experiments detected cell viability, proliferation, migration, and invasion. The effect of ITGBL1 on COAD tumor growth was examined using a xenograft tumor model. The effects of COAD cells on macrophage polarization and the proliferation and apoptosis of CD8+ T cells were analyzed using flow cytometry analysis. Relationships between RBM15 and ITGBL1 were validated using MeRIP and dual-luciferase reporter assay.</p><p><strong>Results: </strong>ITGBL1 and RBM15 contents were elevated in COAD. ITGBL1 knockdown could hinder COAD cell proliferation, migration, invasion, M2-type macrophage polarization, and lymphocyte immunity. Meanwhile, the lack of RBM15 dampened tumor growth in vivo. Mechanistically, RBM15 could increase ITGBL1 expression by m6A methylation.</p><p><strong>Conclusion: </strong>RBM15 could promote COAD progression by regulating ITGBL1 mRNA stability, providing a promising biomarker and a potential target for COAD.</p>\",\"PeriodicalId\":51205,\"journal\":{\"name\":\"Turkish Journal of Gastroenterology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":1.4000,\"publicationDate\":\"2025-01-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Turkish Journal of Gastroenterology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5152/tjg.2025.24068\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Turkish Journal of Gastroenterology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5152/tjg.2025.24068","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

背景/目的:结肠腺癌(COAD)是一种常见的消化系统恶性肿瘤。已有研究表明,RNA n6 -甲基腺苷(m6A)甲基转移酶RNA结合基序蛋白-15 (RBM15)参与多种癌症的发生。我们旨在研究RBM15在COAD进展中的功能及其潜在的分子机制。材料和方法:应用TIMER和UALCAN数据库分析COAD与整合素β样1蛋白(Integrin β-like 1 protein, ITGBL1)或RBM15的关系。采用RT-qPCR和Western blot分析ITGBL1、m2型巨噬细胞标志物、emt相关标志物和RBM15表达。CCK-8、菌落形成和transwell实验检测细胞活力、增殖、迁移和侵袭。采用异种移植肿瘤模型检测ITGBL1对COAD肿瘤生长的影响。采用流式细胞术分析COAD细胞对巨噬细胞极化、CD8+ T细胞增殖和凋亡的影响。RBM15和ITGBL1之间的关系通过MeRIP和双荧光素酶报告试验验证。结果:COAD患者ITGBL1、RBM15含量升高。ITGBL1敲低可抑制COAD细胞的增殖、迁移、侵袭、m2型巨噬细胞极化和淋巴细胞免疫。同时,体内缺乏RBM15抑制肿瘤生长。机制上,RBM15可以通过m6A甲基化增加ITGBL1的表达。结论:RBM15可通过调控ITGBL1 mRNA的稳定性促进COAD的进展,为COAD提供了一种有前景的生物标志物和潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment.

Background/aims: Colon adenocarcinoma (COAD) is a prevalent malignant tumor of the digestive system. Previous research has indicated that RNA N6-methyladenosine (m6A) methyltransferase RNA-binding motif protein-15 (RBM15) is involved in various cancers. We aimed to investigate the function of RBM15 in COAD progression and its underlying molecular mechanism.

Materials and methods: TIMER and UALCAN databases were applied to analyze the relationship between COAD and Integrin β-like 1 protein (ITGBL1) or RBM15. RT-qPCR and Western blot were used to analyze ITGBL1, M2-type macrophage markers, EMT-related markers, and RBM15 expression. CCK-8, colony formation, and transwell experiments detected cell viability, proliferation, migration, and invasion. The effect of ITGBL1 on COAD tumor growth was examined using a xenograft tumor model. The effects of COAD cells on macrophage polarization and the proliferation and apoptosis of CD8+ T cells were analyzed using flow cytometry analysis. Relationships between RBM15 and ITGBL1 were validated using MeRIP and dual-luciferase reporter assay.

Results: ITGBL1 and RBM15 contents were elevated in COAD. ITGBL1 knockdown could hinder COAD cell proliferation, migration, invasion, M2-type macrophage polarization, and lymphocyte immunity. Meanwhile, the lack of RBM15 dampened tumor growth in vivo. Mechanistically, RBM15 could increase ITGBL1 expression by m6A methylation.

Conclusion: RBM15 could promote COAD progression by regulating ITGBL1 mRNA stability, providing a promising biomarker and a potential target for COAD.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Turkish Journal of Gastroenterology
Turkish Journal of Gastroenterology 医学-胃肠肝病学
CiteScore
1.90
自引率
0.00%
发文量
127
审稿时长
6 months
期刊介绍: The Turkish Journal of Gastroenterology (Turk J Gastroenterol) is the double-blind peer-reviewed, open access, international publication organ of the Turkish Society of Gastroenterology. The journal is a bimonthly publication, published on January, March, May, July, September, November and its publication language is English. The Turkish Journal of Gastroenterology aims to publish international at the highest clinical and scientific level on original issues of gastroenterology and hepatology. The journal publishes original papers, review articles, case reports and letters to the editor on clinical and experimental gastroenterology and hepatology.
期刊最新文献
Impact of Caudate Lobe Resection on Overall Survival and Liver Disease-Free Survival in Colorectal Liver Metastases: A Pilot Study. Matrine Alleviates Oxidative Stress and Inflammation in Colon Cancer by Activating the Nrf2 Pathway. Integrated Analysis of Gut Microbiota and Metabolites in a Rat Necrotizing Enterocolitis Model. Long Non-Coding RNA LINC01123 Facilitates Cholangiocarcinoma Aggravation by Targeting miR-641. m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1