Solasonine Restores Sensitivity of Gastric Cancer to NK Cells through DNA Demethylation of MICA.

IF 2.6 3区 生物学 Q3 MATERIALS SCIENCE, BIOMATERIALS
Tianchuan Li, Ailian Yang, Bingjing He, Zhifeng Zhou, Danhong Wu, Yunqing Xie
{"title":"Solasonine Restores Sensitivity of Gastric Cancer to NK Cells through DNA Demethylation of MICA.","authors":"Tianchuan Li, Ailian Yang, Bingjing He, Zhifeng Zhou, Danhong Wu, Yunqing Xie","doi":"10.1002/adbi.202400793","DOIUrl":null,"url":null,"abstract":"<p><p>Solasonine, extracted from Solanum nigrum, has been proven to exert anti-tumor effects in various tumors. However, the role of solasonine in gastric cancer remains unclear. This study aims to elucidate the therapeutic effects of solasonine in suppressing gastric cancer progression. This study explores the regulatory mechanism of solasonine in vitro cells and xenograft tumor mouse models. Methylation-specific PCR (MSP) is used for DNA methylation analysis; immunohistochemical and flow cytometry are performed for MHC class I polypeptide-related sequence A (MICA) expression profiling. Solasonine inhibits the proliferation and migration of gastric cancer cells. MICA is identified as a regulatory target for solasonine in gastric cancer cells. Mechanistically, DNA methylation of MICA is suppressed by solasonine. DNA methyltransferases (DNMT) family members, DNMT1, DNMT3A, and DNMT3B, are downregulated in solasonine-treated tumor tissues. Importantly, solasonine restores the sensitivity of HGC-27 cells to natural killer (NK) cells through upregulating MICA, suggesting the potential value of solasonine as an immunotherapy drug in gastric cancer. Solasonine inhibits gastric cancer progression and restores sensitivity of gastric cancer to NK cells through inducing DNA demethylation of the MICA promoter in vitro and in vivo. This study provides application prospects for solasonine anti-tumor therapy.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e00793"},"PeriodicalIF":2.6000,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advanced biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1002/adbi.202400793","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 0

Abstract

Solasonine, extracted from Solanum nigrum, has been proven to exert anti-tumor effects in various tumors. However, the role of solasonine in gastric cancer remains unclear. This study aims to elucidate the therapeutic effects of solasonine in suppressing gastric cancer progression. This study explores the regulatory mechanism of solasonine in vitro cells and xenograft tumor mouse models. Methylation-specific PCR (MSP) is used for DNA methylation analysis; immunohistochemical and flow cytometry are performed for MHC class I polypeptide-related sequence A (MICA) expression profiling. Solasonine inhibits the proliferation and migration of gastric cancer cells. MICA is identified as a regulatory target for solasonine in gastric cancer cells. Mechanistically, DNA methylation of MICA is suppressed by solasonine. DNA methyltransferases (DNMT) family members, DNMT1, DNMT3A, and DNMT3B, are downregulated in solasonine-treated tumor tissues. Importantly, solasonine restores the sensitivity of HGC-27 cells to natural killer (NK) cells through upregulating MICA, suggesting the potential value of solasonine as an immunotherapy drug in gastric cancer. Solasonine inhibits gastric cancer progression and restores sensitivity of gastric cancer to NK cells through inducing DNA demethylation of the MICA promoter in vitro and in vivo. This study provides application prospects for solasonine anti-tumor therapy.

茄碱通过MICA DNA去甲基化恢复胃癌对NK细胞的敏感性。
从茄属植物中提取的茄碱已被证实对多种肿瘤具有抗肿瘤作用。然而,茄碱在胃癌中的作用尚不清楚。本研究旨在阐明茄碱在抑制胃癌进展中的治疗作用。本研究探讨茄碱在体外细胞和异种移植瘤小鼠模型中的调节机制。甲基化特异性PCR (MSP)用于DNA甲基化分析;免疫组织化学和流式细胞术检测MHC I类多肽相关序列A (MICA)表达谱。茄碱抑制胃癌细胞的增殖和迁移。MICA被确定为胃癌细胞中茄碱的调控靶点。机理上,MICA的DNA甲基化被茄碱抑制。DNA甲基转移酶(DNMT)家族成员DNMT1、DNMT3A和DNMT3B在茄碱治疗的肿瘤组织中下调。重要的是,茄碱通过上调MICA,恢复HGC-27细胞对自然杀伤(NK)细胞的敏感性,提示茄碱作为胃癌免疫治疗药物的潜在价值。在体外和体内,茄碱通过诱导MICA启动子的DNA去甲基化,抑制胃癌的进展,恢复胃癌对NK细胞的敏感性。本研究为茄碱抗肿瘤治疗提供了应用前景。
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
Advanced biology
Advanced biology Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
6.60
自引率
0.00%
发文量
130
×
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