前列腺癌中表观遗传学与促肿瘤雄激素信号传导的串扰。

4区 医学 Q3 Biochemistry, Genetics and Molecular Biology
Vipendra Kumar Singh, K M Kainat, Pradeep Kumar Sharma
{"title":"前列腺癌中表观遗传学与促肿瘤雄激素信号传导的串扰。","authors":"Vipendra Kumar Singh,&nbsp;K M Kainat,&nbsp;Pradeep Kumar Sharma","doi":"10.1016/bs.vh.2022.11.007","DOIUrl":null,"url":null,"abstract":"<p><p>Prostate cancer (PCa) is one of the major health burdens among all cancer types in men globally. Early diagnosis and efficacious treatment options are highly warranted as far as the incidence of PCa is concerned. Androgen-dependent transcriptional activation of androgen receptor (AR) is central to the prostate tumorigenesis and therefore hormonal ablation therapy remains the first line of treatment for PCa in the clinics. However, the molecular signaling engaged in AR-dependent PCa initiation and progression is infrequent and diverse. Moreover, apart from the genomic changes, non-genomic changes such as epigenetic modifications have also been suggested as critical regulator of PCa development. Among the non-genomic mechanisms, various epigenetic changes such as histones modifications, chromatin methylation and noncoding RNAs regulations etc. play decisive role in the prostate tumorigenesis. Given that epigenetic modifications are reversible using pharmacological modifiers, various promising therapeutic approaches have been designed for the better management of PCa. In this chapter, we discuss the epigenetic control of tumor promoting AR signaling that underlies the mechanism of prostate tumorigenesis and progression. In addition, we have discussed the approaches and opportunities to develop novel epigenetic modifications based therapeutic strategies for targeting PCa including castrate resistant prostate cancer (CRPC).</p>","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"122 ","pages":"253-282"},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Crosstalk between epigenetics and tumor promoting androgen signaling in prostate cancer.\",\"authors\":\"Vipendra Kumar Singh,&nbsp;K M Kainat,&nbsp;Pradeep Kumar Sharma\",\"doi\":\"10.1016/bs.vh.2022.11.007\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Prostate cancer (PCa) is one of the major health burdens among all cancer types in men globally. Early diagnosis and efficacious treatment options are highly warranted as far as the incidence of PCa is concerned. Androgen-dependent transcriptional activation of androgen receptor (AR) is central to the prostate tumorigenesis and therefore hormonal ablation therapy remains the first line of treatment for PCa in the clinics. However, the molecular signaling engaged in AR-dependent PCa initiation and progression is infrequent and diverse. Moreover, apart from the genomic changes, non-genomic changes such as epigenetic modifications have also been suggested as critical regulator of PCa development. Among the non-genomic mechanisms, various epigenetic changes such as histones modifications, chromatin methylation and noncoding RNAs regulations etc. play decisive role in the prostate tumorigenesis. Given that epigenetic modifications are reversible using pharmacological modifiers, various promising therapeutic approaches have been designed for the better management of PCa. In this chapter, we discuss the epigenetic control of tumor promoting AR signaling that underlies the mechanism of prostate tumorigenesis and progression. In addition, we have discussed the approaches and opportunities to develop novel epigenetic modifications based therapeutic strategies for targeting PCa including castrate resistant prostate cancer (CRPC).</p>\",\"PeriodicalId\":51209,\"journal\":{\"name\":\"Vitamins and Hormones\",\"volume\":\"122 \",\"pages\":\"253-282\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Vitamins and Hormones\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/bs.vh.2022.11.007\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Vitamins and Hormones","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/bs.vh.2022.11.007","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0

摘要

前列腺癌(PCa)是全球男性所有癌症类型中的主要健康负担之一。就前列腺癌的发病率而言,早期诊断和有效的治疗方案是非常必要的。雄激素受体(AR)的雄激素依赖性转录激活是前列腺肿瘤发生的核心,因此激素消融治疗仍然是临床治疗前列腺癌的一线治疗方法。然而,参与ar依赖性PCa起始和进展的分子信号并不常见且多样。此外,除了基因组变化外,表观遗传修饰等非基因组变化也被认为是PCa发展的关键调节因子。在非基因组机制中,组蛋白修饰、染色质甲基化、非编码rna调控等各种表观遗传变化在前列腺肿瘤发生中起决定性作用。鉴于表观遗传修饰是可逆的使用药理学调节剂,各种有希望的治疗方法已经设计为更好地管理PCa。在本章中,我们讨论了肿瘤促进AR信号的表观遗传控制,这是前列腺肿瘤发生和发展机制的基础。此外,我们还讨论了开发新的基于表观遗传修饰的靶向前列腺癌治疗策略的方法和机会,包括去势抵抗性前列腺癌(CRPC)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Crosstalk between epigenetics and tumor promoting androgen signaling in prostate cancer.

Prostate cancer (PCa) is one of the major health burdens among all cancer types in men globally. Early diagnosis and efficacious treatment options are highly warranted as far as the incidence of PCa is concerned. Androgen-dependent transcriptional activation of androgen receptor (AR) is central to the prostate tumorigenesis and therefore hormonal ablation therapy remains the first line of treatment for PCa in the clinics. However, the molecular signaling engaged in AR-dependent PCa initiation and progression is infrequent and diverse. Moreover, apart from the genomic changes, non-genomic changes such as epigenetic modifications have also been suggested as critical regulator of PCa development. Among the non-genomic mechanisms, various epigenetic changes such as histones modifications, chromatin methylation and noncoding RNAs regulations etc. play decisive role in the prostate tumorigenesis. Given that epigenetic modifications are reversible using pharmacological modifiers, various promising therapeutic approaches have been designed for the better management of PCa. In this chapter, we discuss the epigenetic control of tumor promoting AR signaling that underlies the mechanism of prostate tumorigenesis and progression. In addition, we have discussed the approaches and opportunities to develop novel epigenetic modifications based therapeutic strategies for targeting PCa including castrate resistant prostate cancer (CRPC).

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
Vitamins and Hormones
Vitamins and Hormones 医学-内分泌学与代谢
CiteScore
3.80
自引率
0.00%
发文量
66
审稿时长
6-12 weeks
期刊介绍: First published in 1943, Vitamins and Hormones is the longest-running serial published by Academic Press. In the early days of the serial, the subjects of vitamins and hormones were quite distinct. The Editorial Board now reflects expertise in the field of hormone action, vitamin action, X-ray crystal structure, physiology, and enzyme mechanisms. Vitamins and Hormones continues to publish cutting-edge reviews of interest to endocrinologists, biochemists, nutritionists, pharmacologists, cell biologists, and molecular biologists. Others interested in the structure and function of biologically active molecules like hormones and vitamins will, as always, turn to this series for comprehensive reviews by leading contributors to this and related disciplines.
×
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