Involvement of STAT3 in immune evasion during lung tumorigenesis

被引：29

作者：

Kida, Hiroshi ^{[1
]}

Ihara, Shoichi ^{[1
]}

Kumanogoh, Atsushi ^{[1
,2
]}

机构：

[1] Osaka Univ, Dept Resp Med Allergy & Rheumat Dis, Grad Sch Med, Suita, Osaka, Japan

[2] Osaka Univ, CREST, Japan Sci & Technol Agcy JST, Grad Sch Med, Suita, Osaka, Japan

来源：

ONCOIMMUNOLOGY | 2013年 / 2卷 / 01期

关键词：

antitumor immunity; lung; MHC Class I; MICA; NK cell; STAT3; tumorigenesis; CANCER; CELLS;

D O I：

10.4161/onci.22653

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

In a recent study, we have shown that STAT3 expressed by tumor cells blunts antitumor immunity during carcinogen-induced lung tumorigenesis. STAT3 inhibits the production of pro-inflammatory chemokines and MHC Class I chain-related gene A. In contrast, STAT3 promotes the expression of MHC Class I molecules. Consequently, STAT3 promotes tumor cell resistance to NK cell-mediated cytotoxicity.

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页数：2

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