BCL6 represses smad signaling in transforming growth factor-β resistance

被引：28

作者：

Wang, Degang ^{[1
]}

Long, Jianyin ^{[1
]}

Dai, Fangyan ^{[1
,2
]}

Liang, Min ^{[1
]}

Feng, Xin-Hua ^{[1
,2
]}

Lin, Xia ^{[1
]}

机构：

[1] Baylor Coll Med, Michael E DeBakey Dept Surg, Houston, TX 77030 USA

[2] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA

来源：

CANCER RESEARCH | 2008年 / 68卷 / 03期

关键词：

D O I：

10.1158/0008-5472.CAN-07-0008

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Transforming growth factor-beta (TGF-beta) controls a wide spectrum of cellular processes. Deregulation of TGF-beta signaling contributes to the pathogenesis of many diseases including cancer and autoimmune diseases. TGF-beta signaling is generally mediated through intracellular signal transducers and transcription factors called Smads. Herein, we have identified the oncoprotein BCL6 as a transcriptional corepressor of tumor suppressor Smad4. BCL6 physically interacts with Smad3 and Smad4, disrupts the Smad-p300 interaction, and represses the transcriptional activity of Smad4. In accordance, B-cell lymphoma cells with a high expression level of BCL6 were found to be refractory to TGF-beta antiproliferative response, whereas knockdown of BCL6 expression in B-cell lymphoma cells partially restores the TGF-beta responses. This study provides strong evidence that overexpression of BCL6 contributes to TGF-beta resistance in B-cell lymphoma.

引用

页码：783 / 789

页数：7

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