The Role of TRPM2 Channel in Doxorubicin-induced Cell Damage in Laryngeal Squamous Cancer Cells.

IF 0.8 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Tarık Yağcı, Ramazan Çınar, Halil İbrahim Altıner, Rıza Dündar, Kenan Yıldızhan
{"title":"The Role of TRPM2 Channel in Doxorubicin-induced Cell Damage in Laryngeal Squamous Cancer Cells.","authors":"Tarık Yağcı, Ramazan Çınar, Halil İbrahim Altıner, Rıza Dündar, Kenan Yıldızhan","doi":"10.1134/S1607672924601070","DOIUrl":null,"url":null,"abstract":"<p><p>Laryngeal squamous cell carcinoma is a common type of head and neck cancer. This study investigated the role of the TRPM2 channel in doxorubicin (DOX)-induced cell damage in human laryngeal squamous cancer cells (Hep-2). Cells were exposed to various DOX concentrations and the appropriate dose was found. Then, TRPM2 antagonist ACA was treated. At the end of the study, cell viability test, Western blot and oxidative stress and inflammatory markers were examined. The results showed that TRPM2 channel expression increased with DOX administration, and DOX incubation in cells caused an increase in ROS, MDA, IL-1β, IL-6, and TNF-α levels, while GSH and GSH-Px levels decreased. Concurrent treatment with ACA attenuated these effects and reduced oxidative stress and inflammation. In addition, DOX-induced apoptosis markers including Casp-3, Casp-8, Casp-9, p53, and Bax were elevated, while Bcl-2 levels were decreased; ACA treatment reversed these changes. The study demonstrated that DOX treatment significantly enhances TRPM2 channel activation and ROS production in Hep-2 cells, thereby initiating apoptotic pathways that lead to cell death. Consequently, targeting the TRPM2 channel may represent a promising therapeutic strategy for treating laryngeal cancer.</p>","PeriodicalId":529,"journal":{"name":"Doklady Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":0.8000,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Doklady Biochemistry and Biophysics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1134/S1607672924601070","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Laryngeal squamous cell carcinoma is a common type of head and neck cancer. This study investigated the role of the TRPM2 channel in doxorubicin (DOX)-induced cell damage in human laryngeal squamous cancer cells (Hep-2). Cells were exposed to various DOX concentrations and the appropriate dose was found. Then, TRPM2 antagonist ACA was treated. At the end of the study, cell viability test, Western blot and oxidative stress and inflammatory markers were examined. The results showed that TRPM2 channel expression increased with DOX administration, and DOX incubation in cells caused an increase in ROS, MDA, IL-1β, IL-6, and TNF-α levels, while GSH and GSH-Px levels decreased. Concurrent treatment with ACA attenuated these effects and reduced oxidative stress and inflammation. In addition, DOX-induced apoptosis markers including Casp-3, Casp-8, Casp-9, p53, and Bax were elevated, while Bcl-2 levels were decreased; ACA treatment reversed these changes. The study demonstrated that DOX treatment significantly enhances TRPM2 channel activation and ROS production in Hep-2 cells, thereby initiating apoptotic pathways that lead to cell death. Consequently, targeting the TRPM2 channel may represent a promising therapeutic strategy for treating laryngeal cancer.

TRPM2通道在阿霉素诱导的喉癌细胞损伤中的作用。
喉部鳞状细胞癌是一种常见的头颈部癌症。本研究探讨了TRPM2通道在阿霉素(DOX)诱导的人喉鳞癌细胞(Hep-2)损伤中的作用。细胞暴露于不同的DOX浓度,并找到合适的剂量。然后给予TRPM2拮抗剂ACA治疗。研究结束时进行细胞活力、免疫印迹、氧化应激和炎症标志物检测。结果显示,TRPM2通道表达随DOX处理增加,DOX在细胞内孵养引起ROS、MDA、IL-1β、IL-6和TNF-α水平升高,GSH和GSH- px水平降低。与ACA同时治疗可减轻这些影响,并减少氧化应激和炎症。此外,dox诱导的凋亡标志物Casp-3、Casp-8、Casp-9、p53、Bax水平升高,Bcl-2水平降低;ACA治疗逆转了这些变化。研究表明,DOX处理显著增强Hep-2细胞中TRPM2通道激活和ROS产生,从而启动凋亡途径,导致细胞死亡。因此,靶向TRPM2通道可能是治疗喉癌的一种有希望的治疗策略。
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
Doklady Biochemistry and Biophysics
Doklady Biochemistry and Biophysics 生物-生化与分子生物学
CiteScore
1.60
自引率
12.50%
发文量
68
审稿时长
6-12 weeks
期刊介绍: Doklady Biochemistry and Biophysics is a journal consisting of English translations of articles published in Russian in biochemistry and biophysics sections of the Russian-language journal Doklady Akademii Nauk. The journal''s goal is to publish the most significant new research in biochemistry and biophysics carried out in Russia today or in collaboration with Russian authors. The journal accepts only articles in the Russian language that are submitted or recommended by acting Russian or foreign members of the Russian Academy of Sciences. The journal does not accept direct submissions in English.
×
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:481959085
Book学术官方微信