Novel activators and small-molecule inhibitors of STAT3 in cancer

被引:103
作者
Yang, Lehe [1 ,2 ,3 ]
Lin, Shichong [1 ,2 ]
Xu, Lingyuan [1 ,2 ]
Lin, Jiayuh [3 ]
Zhao, Chengguang [2 ]
Huang, Xiaoying [1 ]
机构
[1] Wenzhou Med Univ, Affiliated Hosp 1, Dept Resp Med, Wenzhou 325000, Zhejiang, Peoples R China
[2] Wenzhou Med Univ, Chem Biol Res Ctr, Sch Pharmaceut Sci, Bldg 11,Chashan St, Wenzhou 325035, Zhejiang, Peoples R China
[3] Univ Maryland, Sch Med, Dept Biochem & Mol Biol, Baltimore, MD 21201 USA
关键词
STAT3; Activator; Cancer; Signal pathway; Inhibitor; CELL LUNG-CANCER; NF-KAPPA-B; TUMOR ANGIOGENESIS; TRANSCRIPTION; SIGNAL TRANSDUCER; VEGF EXPRESSION; IN-VITRO; PROMOTES; APOPTOSIS; ACID;
D O I
10.1016/j.cytogfr.2019.10.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Excessive activation of signal transducer and activator of transcription 3 (STAT3) signaling is observed in a subset of many cancers, making activated STAT3 a highly promising potential therapeutic target supported by multiple preclinical and clinical studies. However, early-phase clinical trials have produced mixed results with STAT3-targeted cancer therapies, revealing substantial complexity to targeting aberrant STAT3 signaling. This review discusses the diverse mechanisms of oncogenic activation of STAT3, and the small molecule inhibitors of STAT3 in cancer treatment.
引用
收藏
页码:10 / 22
页数:13
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