STAT and SMAD signaling in cancer

• T. Iwamoto ^[1] ; K. Oshima ^[1] ; T. Senga ^[1] ; X. Feng ^[1] ; M.L. Oo ^[1] ; M. Hamaguchi ^[1] ; S. Matsuda ^[1]
  1. [1] Nagoya University

     Nagoya University

     Naka-ku, Japón

     
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 17, Nº. 3, 2002, págs. 887-895
• Idioma: inglés
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• Resumen

  • STAT and SMAD often exert opposite biological effects on diverse cellular functions. Recent studies have shown that STAT can interface with SMAD at molecular level and that some novel molecules, such as SOCS (also called CIS) and APRO6 (also called TOB), modulate this signaling. A cofactor p300/CBP might act as a bridging molecule to mediate the interface. Thus, STAT and SMAD signaling pathways may crosstalk each other with interweaved regulatory mechanisms. Interestingly, the importance of all the proteins' function has been shown by the increasing evidence of their involvement in cancer. These recent progresses have been made in attributing novel exciting functions. Accordingly, we would like to review the latest advances of those pathways on a cross-section in cancer signaling