Activation of p53 by specific agents in potential cancer therapy.

John W Ho, Jing Zheng Song, Yuet Kin Leung
{"title":"Activation of p53 by specific agents in potential cancer therapy.","authors":"John W Ho,&nbsp;Jing Zheng Song,&nbsp;Yuet Kin Leung","doi":"10.2174/1568011053174819","DOIUrl":null,"url":null,"abstract":"<p><p>Tumor suppressor genes can promote p53-mediated apoptosis. Apoptosis is an important protective mechanism for normal cell growth. Aberrant regulation of p53 expression is linked to cancer development. The loss of function of p53 often results in tumorigenicity. It is reported that the high incidence of tumors in p53-deficient animals is highly attributed to p53-induced apoptosis. Malignancies that retain the wild-type p53 gene are associated with the biologic activity of p53 function. Most cancer cells show defects in p53 or inhibition in the associated pathways. A lot of effort has been focused on reactivating mutant p53, or recombinant technique to incorporate p53 in cells. Regulation of p53 has been described at both transcription and translation level. Activation of the p53 pathway appears to be an effective approach in inhibiting tumor development. In the present study, we have reviewed the recent developments of specific compounds that can regulate p53 expression and its function in cell growth and development. Integral to this is the function of other proteins that affect p53 activity.</p>","PeriodicalId":10914,"journal":{"name":"Current medicinal chemistry. Anti-cancer agents","volume":"5 2","pages":"131-5"},"PeriodicalIF":0.0000,"publicationDate":"2005-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568011053174819","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current medicinal chemistry. Anti-cancer agents","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1568011053174819","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9

Abstract

Tumor suppressor genes can promote p53-mediated apoptosis. Apoptosis is an important protective mechanism for normal cell growth. Aberrant regulation of p53 expression is linked to cancer development. The loss of function of p53 often results in tumorigenicity. It is reported that the high incidence of tumors in p53-deficient animals is highly attributed to p53-induced apoptosis. Malignancies that retain the wild-type p53 gene are associated with the biologic activity of p53 function. Most cancer cells show defects in p53 or inhibition in the associated pathways. A lot of effort has been focused on reactivating mutant p53, or recombinant technique to incorporate p53 in cells. Regulation of p53 has been described at both transcription and translation level. Activation of the p53 pathway appears to be an effective approach in inhibiting tumor development. In the present study, we have reviewed the recent developments of specific compounds that can regulate p53 expression and its function in cell growth and development. Integral to this is the function of other proteins that affect p53 activity.

在潜在的癌症治疗中,特定药物激活p53。
肿瘤抑制基因可促进p53介导的细胞凋亡。细胞凋亡是细胞正常生长的重要保护机制。p53表达的异常调控与癌症的发展有关。p53功能的丧失常常导致致瘤性。据报道,p53缺陷动物中肿瘤的高发生率与p53诱导的细胞凋亡高度相关。保留野生型p53基因的恶性肿瘤与p53功能的生物活性有关。大多数癌细胞表现出p53的缺陷或相关通路的抑制。很多努力都集中在重新激活突变的p53,或重组技术将p53纳入细胞中。p53的调控已经在转录和翻译水平上被描述。激活p53通路似乎是抑制肿瘤发展的有效途径。在本研究中,我们综述了近年来调控p53表达及其在细胞生长发育中的作用的特异性化合物的研究进展。与此相关的是影响p53活性的其他蛋白质的功能。
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
自引率
0.00%
发文量
0
×
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