STAT3 SIGNALING: Anticancer Strategies and Challenges

被引：363

作者：

Johnston, Paul A. ^{[3
,4
]}

Grandis, Jennifer R. ^{[1
,2
]}

机构：

[1] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15260 USA

[2] Univ Pittsburgh, Sch Med, Dept Otolaryngol, Pittsburgh, PA USA

[3] Sch Med, Sch Pharmaceut Sci, Pittsburgh, PA USA

[4] Univ Pittsburgh, Sch Med, Drug Discovery Inst, Pittsburgh, PA USA

来源：

MOLECULAR INTERVENTIONS | 2011年 / 11卷 / 01期

基金：

美国国家卫生研究院;

关键词：

GROWTH-FACTOR RECEPTOR; NECK-CANCER; JAK2; INHIBITOR; TRANSDUCER; ACTIVATOR; TRANSCRIPTION-3; KINASE; HEAD; PROTEIN; PATHWAYS;

D O I：

10.1124/mi.11.1.4

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Multiple lines of evidence place STAT3 at a central node in the development, progression, and maintenance of many human tumors, and STAT3 has been validated as an anticancer target in several contexts. STAT3 modulates the transcription of a variety of genes involved in the regulation of critical functions, including cell differentiation, proliferation, apoptosis, angiogenesis, metastasis, and immune responses. For many cancers, elevated levels of activated STAT3 have been associated with a poor prognosis. We review approaches that have been pursued to target STAT3, and we highlight some of the promises and challenges associated with developing an anticancer drug that might therapeutically inhibit the STAT3 signaling pathway.

引用

页码：18 / 26

页数：9

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