Article(id=1291707060471751109, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.24.016, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1760544000000, receivedDateStr=2025-10-16, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896561972, onlineDateStr=2026-08-05, pubDate=1766851200000, pubDateStr=2025-12-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896561972, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896561972, creator=13701087609, updateTime=1785896561972, updator=13701087609, issue=Issue{id=1291706966187991876, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='24', pageStart='3451', pageEnd='3600', issueExtLink='null', onlineDate='null', pubDate='1766851200000', pubDateStr='2025-12-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896539494, creator='13701087609', updateTime=1785998798662, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292135872292479273, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292135872296673578, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706966187991876, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3548, endPage=3554, ext={EN=ArticleExt(id=1291707060920541638, articleId=1291707060471751109, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=The role of Stat3 phosphorylation in tumorigenesis and tumor development, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Signal transducer and activator of transcription 3 (Stat3), as a crucial transcription factor, plays a core regulatory role in regulating the cell cycle and various cellular processes such as proliferation, survival, differentiation, and inflammatory responses. Aberrant activation of Stat3 is closely related to the occurrence and development of many tumors. Meanwhile, the activity and stability of Stat3 are influenced by its post-translational modifications, including phosphorylation, acetylation, methylation, etc., among which phosphorylation is one of the most critical regulatory mechanisms. Under pathological and physiological stimuli, phosphorylation modifications can alter the structure of Stat3 in different cells, thereby determining specific gene programs. This process leads to the activation of Stat3 and promotes tumor cell proliferation, etc. This article focuses on the phosphorylation modification of Stat3, systematically elaborating on the regulatory mechanisms of its main phosphorylation sites (tyrosine 705 site and serine 727 site), as well as its roles in tumor cell cycle regulation, apoptosis inhibition, angiogenesis, invasion and metastasis, and tumor microenvironment remodeling. At the same time, it explores tumor treatment strategies targeting Stat3 phosphorylation, providing theoretical references for tumor mechanism research and clinical treatment.

, authors=Jia-xu CHEN, Xu-tao SUN, Ning HAN, Cai-yun MAO, Yun-jia SONG, authorsList=Jia-xu CHEN, Xu-tao SUN, Ning HAN, Cai-yun MAO, Yun-jia SONG, authorCompany=null, correspAuthors=Yun-jia SONG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291707062132695495, articleId=1291707060471751109, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=Stat3磷酸化在肿瘤发生发展中的作用, columnId=1246531408819278046, journalTitle=中国临床药理学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

信号传导与转录激活因子3（Stat3）作为一种十分关键的转录因子，在调节细胞周期以及细胞的增殖、存活、分化及炎症反应等过程中起着核心调控作用，其异常激活与多种肿瘤的发生发展密切相关。同时，Stat3的活性与稳定性受其翻译后修饰的影响，常见的修饰类型有磷酸化、乙酰化、甲基化等，其中磷酸化是最关键的调控方式之一。在病理生理刺激下，磷酸化修饰会改变Stat3在不同细胞中的结构，进而决定特定的基因程序。这一过程会使Stat3发生活化进而促进肿瘤细胞增殖等。本文聚焦Stat3磷酸化修饰，系统阐述其主要磷酸化位点（酪氨酸705位点、丝氨酸727位点）的调控机制，及其在肿瘤细胞周期调控、抑制凋亡、血管生成、侵袭转移以及肿瘤微环境重塑中的作用，同时探讨以Stat3磷酸化为靶点的肿瘤治疗策略，为肿瘤机制研究与临床治疗提供理论参考。

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陈佳旭（2001-），男，硕士研究生，主要从事心血管疾病方面的研究

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陈佳旭（2001-），男，硕士研究生，主要从事心血管疾病方面的研究

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