Cross‐talk between IL‐6 and TGF‐β signaling in hepatoma cells

FEBS Letters

Muraguchi, Atsushi¹  Matsuda, Tadashi¹  Kawabata, Masahiro²  Yamamoto, Tetsuya¹  Miyazono, Kohei² 

[1] Department of Immunology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan;Department of Biochemistry, The Cancer Institute of Japanese Foundation for Cancer Research (JFCR), 1-37-1 Kami-ikebukuro, Toshima-ku, Tokyo 170-8455, Japan

关键词: Interleukin-6;    Signal transducer and activator of transcription-3;    Transforming growth factor-β;    Sma- and MAD-related protein;    p300;    Cross-talk;    Transcription;    IL;    interleukin;    TGF;    transforming growth factor;    STAT;    signal transducer and activator of transcription;    LUC;    luciferase;    LIF;    leukemia inhibitory factor;    TβR-I;    TGF-β type I receptor;    Smad;    Sma- and MAD-related protein;    BMP;    bone morphogenetic protein;   

DOI  :  10.1016/S0014-5793(01)02258-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Interleukin-6 (IL-6) is a multifunctional cytokine that plays important roles in the immune system, hematopoiesis, and acute phase reactions. Transforming growth factor-β (TGF-β) also has pleiotropy including the production of acute phase proteins in hepatocytes. To elucidate the cross-talk between IL-6 and TGF-β signaling pathways in hepatic cells, we investigated the effects of TGF-β on IL-6-induced signal transducer and activator of transcription-3 (STAT3) activation in a human hepatoma cell line, Hep3B. IL-6-induced activation of STAT3 activity and STAT3-mediated gene expression were augmented by TGF-β in Hep3B cells. We provide evidence that these activities were due to physical interactions between STAT3 and Sma- and MAD-related protein-3, bridged by p300. These results demonstrate a molecular mechanism of a cross-talk between STAT3 and TGF-β signaling pathways in hepatocytes.

【 授权许可】

Unknown