胰黄素以 GSTP1 为靶标诱导肝癌细胞衰老,并增加肝癌细胞对衰老剂凋亡的敏感性

IF 10.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Redox Biology Pub Date : 2024-08-20 DOI:10.1016/j.redox.2024.103323
Yuxuan Zhang , Biying Xiao , Shuying Yuan , Lele Ding , Yongfu Pan , Yanyu Jiang , Shenghao Sun , Xisong Ke , Lili Cai , Lijun Jia
{"title":"胰黄素以 GSTP1 为靶标诱导肝癌细胞衰老,并增加肝癌细胞对衰老剂凋亡的敏感性","authors":"Yuxuan Zhang ,&nbsp;Biying Xiao ,&nbsp;Shuying Yuan ,&nbsp;Lele Ding ,&nbsp;Yongfu Pan ,&nbsp;Yanyu Jiang ,&nbsp;Shenghao Sun ,&nbsp;Xisong Ke ,&nbsp;Lili Cai ,&nbsp;Lijun Jia","doi":"10.1016/j.redox.2024.103323","DOIUrl":null,"url":null,"abstract":"<div><p>Targeting senescence has emerged as a promising strategy for liver cancer treatment. However, the lack of a safe agent capable of inducing complete senescence and being combined with senolytics poses a limitation. Here, we screened a natural product library and identified tryptanthrin (TRYP) as a potent inducer of cellular senescence in liver cancer cells both <em>in vitro</em> and <em>in vivo</em>. Mechanistically, Glutathione S-transferase P1 (GSTP1), a key regulator for redox homeostasis, was identified as a target protein for TRYP-induced senescence. TRYP directly bound to GSTP1 and inhibited its enzymatic activity, mediating reactive oxygen species (ROS) accumulation, followed by DNA damage response (DDR), consequently contributing to initiating primary senescence. Furthermore, TRYP triggered DNA damage-dependent activation of NF-κB pathway, which evoked senescence-associated secretory phenotype (SASP), thereby leading to senescence reinforcement. Importantly, TRYP exposed the vulnerability of tumor cells and sensitized senescent cells to apoptosis induced by senolytic agent ABT263, a Bcl2 inhibitor. Taken together, our findings reveal that TRYP induces cellular senescence via GSTP1/ROS/DDR/NF-κB/SASP axis, providing a novel potential application in synergizing with senolytic therapy in liver cancer.</p></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"76 ","pages":"Article 103323"},"PeriodicalIF":10.7000,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S221323172400301X/pdfft?md5=552ce016118d2be9c2eda5eb116fabbf&pid=1-s2.0-S221323172400301X-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Tryptanthrin targets GSTP1 to induce senescence and increases the susceptibility to apoptosis by senolytics in liver cancer cells\",\"authors\":\"Yuxuan Zhang ,&nbsp;Biying Xiao ,&nbsp;Shuying Yuan ,&nbsp;Lele Ding ,&nbsp;Yongfu Pan ,&nbsp;Yanyu Jiang ,&nbsp;Shenghao Sun ,&nbsp;Xisong Ke ,&nbsp;Lili Cai ,&nbsp;Lijun Jia\",\"doi\":\"10.1016/j.redox.2024.103323\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Targeting senescence has emerged as a promising strategy for liver cancer treatment. However, the lack of a safe agent capable of inducing complete senescence and being combined with senolytics poses a limitation. Here, we screened a natural product library and identified tryptanthrin (TRYP) as a potent inducer of cellular senescence in liver cancer cells both <em>in vitro</em> and <em>in vivo</em>. Mechanistically, Glutathione S-transferase P1 (GSTP1), a key regulator for redox homeostasis, was identified as a target protein for TRYP-induced senescence. TRYP directly bound to GSTP1 and inhibited its enzymatic activity, mediating reactive oxygen species (ROS) accumulation, followed by DNA damage response (DDR), consequently contributing to initiating primary senescence. Furthermore, TRYP triggered DNA damage-dependent activation of NF-κB pathway, which evoked senescence-associated secretory phenotype (SASP), thereby leading to senescence reinforcement. Importantly, TRYP exposed the vulnerability of tumor cells and sensitized senescent cells to apoptosis induced by senolytic agent ABT263, a Bcl2 inhibitor. Taken together, our findings reveal that TRYP induces cellular senescence via GSTP1/ROS/DDR/NF-κB/SASP axis, providing a novel potential application in synergizing with senolytic therapy in liver cancer.</p></div>\",\"PeriodicalId\":20998,\"journal\":{\"name\":\"Redox Biology\",\"volume\":\"76 \",\"pages\":\"Article 103323\"},\"PeriodicalIF\":10.7000,\"publicationDate\":\"2024-08-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S221323172400301X/pdfft?md5=552ce016118d2be9c2eda5eb116fabbf&pid=1-s2.0-S221323172400301X-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Redox Biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S221323172400301X\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Redox Biology","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S221323172400301X","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

以衰老为靶点已成为治疗肝癌的一种前景广阔的策略。然而,缺乏一种能够诱导完全衰老并能与衰老剂联合使用的安全药物构成了限制。在这里,我们筛选了一个天然产物库,发现色青素(TRYP)既能诱导肝癌细胞衰老,又能诱导肝癌细胞衰老。从机理上讲,谷胱甘肽 S 转移酶 P1(GSTP1)是氧化还原平衡的关键调节因子,被确定为 TRYP 诱导衰老的靶蛋白。TRYP 直接与 GSTP1 结合并抑制其酶活性,介导活性氧(ROS)积累,继而引起 DNA 损伤反应(DDR),从而导致原发性衰老的发生。此外,TRYP 还触发了 DNA 损伤依赖性的 NF-κB 通路激活,从而诱发衰老相关分泌表型(SASP),进而导致衰老强化。重要的是,TRYP暴露了肿瘤细胞的脆弱性,并使衰老细胞对Bcl2抑制剂ABT263诱导的凋亡敏感。综上所述,我们的研究结果表明,TRYP 可通过 GSTP1/ROS/DDR/NF-κB/SASP 轴诱导细胞衰老,为肝癌中的衰老疗法提供了一种新的潜在协同应用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

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
Tryptanthrin targets GSTP1 to induce senescence and increases the susceptibility to apoptosis by senolytics in liver cancer cells

Targeting senescence has emerged as a promising strategy for liver cancer treatment. However, the lack of a safe agent capable of inducing complete senescence and being combined with senolytics poses a limitation. Here, we screened a natural product library and identified tryptanthrin (TRYP) as a potent inducer of cellular senescence in liver cancer cells both in vitro and in vivo. Mechanistically, Glutathione S-transferase P1 (GSTP1), a key regulator for redox homeostasis, was identified as a target protein for TRYP-induced senescence. TRYP directly bound to GSTP1 and inhibited its enzymatic activity, mediating reactive oxygen species (ROS) accumulation, followed by DNA damage response (DDR), consequently contributing to initiating primary senescence. Furthermore, TRYP triggered DNA damage-dependent activation of NF-κB pathway, which evoked senescence-associated secretory phenotype (SASP), thereby leading to senescence reinforcement. Importantly, TRYP exposed the vulnerability of tumor cells and sensitized senescent cells to apoptosis induced by senolytic agent ABT263, a Bcl2 inhibitor. Taken together, our findings reveal that TRYP induces cellular senescence via GSTP1/ROS/DDR/NF-κB/SASP axis, providing a novel potential application in synergizing with senolytic therapy in liver 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
Redox Biology
Redox Biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
19.90
自引率
3.50%
发文量
318
审稿时长
25 days
期刊介绍: Redox Biology is the official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe. It is also affiliated with the International Society for Free Radical Research (SFRRI). This journal serves as a platform for publishing pioneering research, innovative methods, and comprehensive review articles in the field of redox biology, encompassing both health and disease. Redox Biology welcomes various forms of contributions, including research articles (short or full communications), methods, mini-reviews, and commentaries. Through its diverse range of published content, Redox Biology aims to foster advancements and insights in the understanding of redox biology and its implications.
期刊最新文献
Corrigendum to "Complement receptor 3 mediates NADPH oxidase activation and dopaminergic neurodegeneration through a Src-Erk-dependent pathway" [Redox Biol. 14 (2018) 250-260]. Corrigendum to "Genome-wide transcriptional effects of deletions of sulphur metabolism genes in Drosophila melanogaster" [Redox Biol. 36 (2020) 101654]. Aβ1-42 promotes microglial activation and apoptosis in the progression of AD by binding to TLR4 Time-restricted eating reveals a "younger" immune system and reshapes the intestinal microbiome in human. Deficiency of muscle-generated brain-derived neurotrophic factor causes inflammatory myopathy through reactive oxygen species-mediated necroptosis and pyroptosis
×
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