STAT3: A key signaling molecule for converting cold to hot tumors

被引：35

作者：

Hu, Rui ^{[1
]}

Han, Qiuju ^{[1
]}

Zhang, Jian ^{[1
]}

机构：

[1] Shandong Univ, Sch Pharmaceut Sci, Inst Immunopharmaceut Sci, 44 Wenhua West Rd, Jinan 250012, Shandong, Peoples R China

来源：

CANCER LETTERS | 2020年 / 489卷

基金：

中国国家自然科学基金;

关键词：

STAT3; Immunosuppression; Lymphocyte infiltration; Tumor microenvironment; HEPATOCELLULAR-CARCINOMA CELLS; NATURAL-KILLER-CELLS; REGULATORY T-CELLS; SUPPRESSOR-CELLS; VASCULAR LEAKAGE; PROSTATE-CANCER; TARGETING STAT3; TRANSCRIPTION; TGF-BETA; PHASE-I;

D O I：

10.1016/j.canlet.2020.05.035

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Tumors can be classified as cold or hot according to the degree of immune cell infiltration into tumor tissues; cold tumors are insensitive to either chemotherapy or immunotherapy and are associated with poor prognosis. Recent studies have shown that STAT3 signaling molecules hinder the conversion of cold to hot tumors by regulating immunosuppressive molecule secretion and immunosuppressive cell functions. This review aims to present the most recent studies on how STAT3 regulates cold tumor formation and discuss its research status in cancer therapy. We also present insight for designing new therapeutic strategies to "heat" tumors and provide a reference for tumor immunotherapy.

引用

页码：29 / 40

页数：12

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