STAT3 mediates the survival signal in oncogenicras-transfected intestinal epithelial cells

作者: Shinichiro Zushi , Yasuhisa Shinomura , Tatsuya Kiyohara , Yoshiji Miyazaki , Shinya Kondo

DOI: 10.1002/(SICI)1097-0215(19981029)78:3<326::AID-IJC12>3.0.CO;2-4

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摘要: The oncogenic ras mutation is a common and critical step in gastrointestinal carcinogenesis. In previous study, we demonstrated that activated the EGF-related peptide autocrine loop apoptosis resistance observed ras-stimulated cell (IEC-ras cell) was dependent on this loop. STATs (signal transducers activators of transcription), first identified as intracellular signal stimulated by cytokines, are known to also be EGF. However, role survival IEC-ras cells not clear. present demonstrate STAT3 constitutively activation considerably suppressed EGF-specific receptor kinase inhibitor AG1478. We show disruption pathway introduction dominant-negative mutant abolishes against UVC MMC treatment without affecting proliferation. Moreover, expression Bcl-2 Bcl-xL, apoptosis-suppressive proteins, reduced STAT3-transfected cells. Thus, appears an important mediator anti-apoptotic Int. J. Cancer 78:326–330, 1998.© 1998 Wiley-Liss, Inc.

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