STAT1 acts as a tumor promoter for leukemia development

被引：124

作者：

Kovacic, Boris

Stoiber, Dagmar

Moriggl, Richard

Weisz, Eva

Ott, Rene G.

Kreibich, Rita

Levy, David E.

Beug, Hartmut

Freissmuth, Michael

Sexl, Veronika ^{[1
]}

机构：

[1] MUW, Dept Pharmacol, A-1090 Vienna, Austria

[2] LBI CR, A-1090 Vienna, Austria

[3] NYU, Sch Med, Dept Pathol & Microbiol, New York, NY 10016 USA

[4] Inst Mol Pathol, A-1030 Vienna, Austria

来源：

CANCER CELL | 2006年 / 10卷 / 01期

基金：

奥地利科学基金会;

关键词：

D O I：

10.1016/j.ccr.2006.05.025

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The tumor suppressor STAT1 is considered a key regulator of the surveillance of developing tumors. Here, we describe an unexpected tumor-promoting role for STAT1 in leukemia. STAT1(-/-) mice are partially protected from leukemia development, and STAT1(-/-) tumor cells induce leukemia in RAG2(-/-) and immunocompetent mice with increased latency. The low MHC class I protein levels of STAT1(-/-) tumor cells enable efficient NK cell lysis and account for the enhanced tumor clearance. Strikingly, STAT1(-/-) tumor cells acquire increased MHC class I expression upon leukemia progression. These findings define STAT1 as a tumor promoter in leukemia development. Furthermore, we describe the upregulation of MHC class I expression as a general mechanism that allows for the escape of hematopoietic malignancies from immune surveillance.

引用

页码：77 / 87

页数：11

共 54 条

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