低温大气等离子体通过ros介导的PI3K/Akt/mTOR信号通路抑制CAL-62细胞的增殖

IF 1 4区 工程技术 Q3 NUCLEAR SCIENCE & TECHNOLOGY
Fang Liu, Yuanyuan Zhou, Wencheng Song, Hongzhi Wang
{"title":"低温大气等离子体通过ros介导的PI3K/Akt/mTOR信号通路抑制CAL-62细胞的增殖","authors":"Fang Liu, Yuanyuan Zhou, Wencheng Song, Hongzhi Wang","doi":"10.1155/2022/3884695","DOIUrl":null,"url":null,"abstract":"This study aimed to investigate the inhibitory effects of cold atmospheric plasma (CAP) on anaplastic thyroid cancer cells (CAL-62 cells) and to reveal the molecular mechanism. The effects of CAP on CAL-62 cells were evaluated by cell viability, superoxide dismutase activity, apoptosis, cell cycle, and protein expression level, and the role of reactive oxygen species (ROS) produced by plasma was also investigated. The results showed that CAP dose-dependently inhibited cell viability and promotes cell apoptosis and G2/M arrest by increasing cell ROS levels. The activity of superoxide dismutase (SOD) was enhanced by CAP which indicated that the antioxidant system of the cell was activated. Additionally, the ROS produced by CAP can inhibit CAL-62 cell proliferation by inhibiting the PI3K/Akt/mTOR signaling pathway. Therefore, these findings will provide useful support for the application of CAP for treating anaplastic thyroid cancer.","PeriodicalId":21629,"journal":{"name":"Science and Technology of Nuclear Installations","volume":null,"pages":null},"PeriodicalIF":1.0000,"publicationDate":"2022-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Cold Atmospheric Plasma Inhibits the Proliferation of CAL-62 Cells through the ROS-Mediated PI3K/Akt/mTOR Signaling Pathway\",\"authors\":\"Fang Liu, Yuanyuan Zhou, Wencheng Song, Hongzhi Wang\",\"doi\":\"10.1155/2022/3884695\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"This study aimed to investigate the inhibitory effects of cold atmospheric plasma (CAP) on anaplastic thyroid cancer cells (CAL-62 cells) and to reveal the molecular mechanism. The effects of CAP on CAL-62 cells were evaluated by cell viability, superoxide dismutase activity, apoptosis, cell cycle, and protein expression level, and the role of reactive oxygen species (ROS) produced by plasma was also investigated. The results showed that CAP dose-dependently inhibited cell viability and promotes cell apoptosis and G2/M arrest by increasing cell ROS levels. The activity of superoxide dismutase (SOD) was enhanced by CAP which indicated that the antioxidant system of the cell was activated. Additionally, the ROS produced by CAP can inhibit CAL-62 cell proliferation by inhibiting the PI3K/Akt/mTOR signaling pathway. Therefore, these findings will provide useful support for the application of CAP for treating anaplastic thyroid cancer.\",\"PeriodicalId\":21629,\"journal\":{\"name\":\"Science and Technology of Nuclear Installations\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.0000,\"publicationDate\":\"2022-06-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Science and Technology of Nuclear Installations\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1155/2022/3884695\",\"RegionNum\":4,\"RegionCategory\":\"工程技术\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"NUCLEAR SCIENCE & TECHNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science and Technology of Nuclear Installations","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1155/2022/3884695","RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NUCLEAR SCIENCE & TECHNOLOGY","Score":null,"Total":0}
引用次数: 2

摘要

本研究旨在探讨冷大气等离子体(CAP)对间变性甲状腺癌细胞(CAL-62细胞)的抑制作用及其分子机制。通过细胞活力、超氧化物歧化酶活性、细胞凋亡、细胞周期和蛋白表达水平评估CAP对CAL-62细胞的影响,并探讨血浆产生的活性氧(ROS)的作用。结果表明,CAP通过增加细胞ROS水平,呈剂量依赖性地抑制细胞活力,促进细胞凋亡和G2/M阻滞。CAP可增强细胞超氧化物歧化酶(SOD)活性,表明细胞的抗氧化系统被激活。另外,CAP产生的ROS可以通过抑制PI3K/Akt/mTOR信号通路抑制CAL-62细胞的增殖。本研究结果将为CAP在甲状腺间变性癌治疗中的应用提供有益的支持。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cold Atmospheric Plasma Inhibits the Proliferation of CAL-62 Cells through the ROS-Mediated PI3K/Akt/mTOR Signaling Pathway
This study aimed to investigate the inhibitory effects of cold atmospheric plasma (CAP) on anaplastic thyroid cancer cells (CAL-62 cells) and to reveal the molecular mechanism. The effects of CAP on CAL-62 cells were evaluated by cell viability, superoxide dismutase activity, apoptosis, cell cycle, and protein expression level, and the role of reactive oxygen species (ROS) produced by plasma was also investigated. The results showed that CAP dose-dependently inhibited cell viability and promotes cell apoptosis and G2/M arrest by increasing cell ROS levels. The activity of superoxide dismutase (SOD) was enhanced by CAP which indicated that the antioxidant system of the cell was activated. Additionally, the ROS produced by CAP can inhibit CAL-62 cell proliferation by inhibiting the PI3K/Akt/mTOR signaling pathway. Therefore, these findings will provide useful support for the application of CAP for treating anaplastic thyroid cancer.
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
Science and Technology of Nuclear Installations
Science and Technology of Nuclear Installations NUCLEAR SCIENCE & TECHNOLOGY-
CiteScore
2.30
自引率
9.10%
发文量
51
审稿时长
4-8 weeks
期刊介绍: Science and Technology of Nuclear Installations is an international scientific journal that aims to make available knowledge on issues related to the nuclear industry and to promote development in the area of nuclear sciences and technologies. The endeavor associated with the establishment and the growth of the journal is expected to lend support to the renaissance of nuclear technology in the world and especially in those countries where nuclear programs have not yet been developed.
×
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