Terrestrosin D inhibits invasion and induces apoptosis through inhibition of STAT3 in anaplastic thyroid carcinoma

IF 1.1 4区 医学 Q4 TOXICOLOGY
Honglai Zhang, Dawei Sun, Peijie Lei, Jingjing Cheng
{"title":"Terrestrosin D inhibits invasion and induces apoptosis through inhibition of STAT3 in anaplastic thyroid carcinoma","authors":"Honglai Zhang, Dawei Sun, Peijie Lei, Jingjing Cheng","doi":"10.1007/s13273-024-00457-3","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>The prognosis with current management approach of anaplastic thyroid carcinoma (ATC) remains poor, and new effective treatments are greatly needed. Terrestrosin D (TED) is active component of traditional Chinese medicine (TCM) <i>Tribulus terrestris L.</i> with anti-tumor and anti-inflammatory activities. However, it remains unclear about the activity and mechanisms of TED in ATC.</p><h3 data-test=\"abstract-sub-heading\">Objectives</h3><p>In this study, the experimental groups included control, DMSO, TED (2.5 μM), and TED (5 μM). We detected cell viability, invasion, migration, and apoptosis to assess the effects of TED on ATC cells in vitro. Next, we performed western blot to determine apoptosis-related proteins and STAT3 protein expression. In addition, the possible mechanism of TED anti-cancer effects on ATC was preliminarily investigated through network pharmacology.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>These results showed that TED groups could significantly inhibit cell viability, invasion, migration, and colony formation ability, and promote the cell apoptosis, compared with the DMSO group. Besides, TED obviously downregulated the levels of Bcl-2, and STAT3 protein, increased level of Bax and caspase-3 protein. Network pharmacological analysis showed that 27 intersecting genes were obtained by intersecting TED and ATC target gene sets, of which STAT3 had the best correlation.</p><h3 data-test=\"abstract-sub-heading\">Conclusions</h3><p>We found that TED has strong anti-cancer activities on ATC, which could induce cell apoptosis through the regulation of STAT3. This study provides a new idea to treat ATC.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"70 1","pages":""},"PeriodicalIF":1.1000,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & Cellular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s13273-024-00457-3","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background

The prognosis with current management approach of anaplastic thyroid carcinoma (ATC) remains poor, and new effective treatments are greatly needed. Terrestrosin D (TED) is active component of traditional Chinese medicine (TCM) Tribulus terrestris L. with anti-tumor and anti-inflammatory activities. However, it remains unclear about the activity and mechanisms of TED in ATC.

Objectives

In this study, the experimental groups included control, DMSO, TED (2.5 μM), and TED (5 μM). We detected cell viability, invasion, migration, and apoptosis to assess the effects of TED on ATC cells in vitro. Next, we performed western blot to determine apoptosis-related proteins and STAT3 protein expression. In addition, the possible mechanism of TED anti-cancer effects on ATC was preliminarily investigated through network pharmacology.

Results

These results showed that TED groups could significantly inhibit cell viability, invasion, migration, and colony formation ability, and promote the cell apoptosis, compared with the DMSO group. Besides, TED obviously downregulated the levels of Bcl-2, and STAT3 protein, increased level of Bax and caspase-3 protein. Network pharmacological analysis showed that 27 intersecting genes were obtained by intersecting TED and ATC target gene sets, of which STAT3 had the best correlation.

Conclusions

We found that TED has strong anti-cancer activities on ATC, which could induce cell apoptosis through the regulation of STAT3. This study provides a new idea to treat ATC.

Abstract Image

Terrestrosin D 通过抑制 STAT3 抑制无性甲状腺癌的侵袭并诱导其凋亡
背景甲状腺无节细胞癌(ATC)目前的治疗方法预后仍然不佳,亟需新的有效治疗方法。蒺藜素 D(TED)是传统中药蒺藜的活性成分,具有抗肿瘤和抗炎活性。本研究的实验组包括对照组、二甲基亚砜组、TED(2.5 μM)组和 TED(5 μM)组。我们检测了细胞活力、侵袭、迁移和凋亡,以评估 TED 在体外对 ATC 细胞的影响。接着,我们用 Western 印迹法检测了细胞凋亡相关蛋白和 STAT3 蛋白的表达。结果表明,与 DMSO 组相比,TED 组能显著抑制细胞活力、侵袭、迁移和集落形成能力,促进细胞凋亡。此外,TED能明显降低Bcl-2和STAT3蛋白的水平,提高Bax和caspase-3蛋白的水平。网络药理学分析表明,TED与ATC靶基因组交叉得到27个交叉基因,其中STAT3的相关性最好。这项研究为治疗 ATC 提供了新思路。
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
CiteScore
2.50
自引率
17.60%
发文量
114
审稿时长
6-12 weeks
期刊介绍: Molecular & Cellular Toxicology publishes original research and reviews in all areas of the complex interaction between the cell´s genome (the sum of all genes within the chromosome), chemicals in the environment, and disease. Acceptable manuscripts are the ones that deal with some topics of environmental contaminants, including those that lie in the domains of analytical chemistry, biochemistry, pharmacology and toxicology with the aspects of molecular and cellular levels. Emphasis will be placed on toxic effects observed at relevant genomics and proteomics, which have direct impact on drug development, environment health, food safety, preventive medicine, and forensic medicine. The journal is committed to rapid peer review to ensure the publication of highest quality original research and timely news and review articles.
×
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