Constitutively activated Stat3 protects fibroblasts from serum withdrawal and UV-induced apoptosis and antagonizes the proapoptotic effects of activated Stat1 Academic Article uri icon

Overview

MeSH Major

  • Apoptosis
  • DNA-Binding Proteins
  • Signal Transduction
  • Trans-Activators

abstract

  • Stats1 and 3 (signal transducers and activators of transcription) can be activated simultaneously, although not necessarily to the same degree or duration, by the interaction of cells with the same polypeptide ligand (EGF, PDGF, or high concentrations of IL-6, for example). However, these two Stat proteins can mediate opposing effects on cell growth and survival. Stat1 activation slows growth and promotes apoptosis. In contrast, activated Stat3 can protect cells from apoptosis. Furthermore, a constitutively active form of Stat3, Stat3-C (bridged by S-S linkages between cysteines instead of phosphotyrosines) can induce cellular transformation of fibroblasts. We have determined that fibroblasts transformed by Stat3-C are more resistant to proapoptotic stimuli than nontransformed cells. Also, to examine the potential opposing roles in apoptosis of Stat1 and Stat3, we studied the cervical carcinoma-derived cell line, Me180, which undergoes Stat1-dependent, IFN gamma-induced apoptosis. Me180 cells that express Stat3-C are protected against IFN gamma-mediated apoptosis.

publication date

  • February 13, 2001

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC29293

Digital Object Identifier (DOI)

  • 10.1073/pnas.041588198

PubMed ID

  • 11171987

Additional Document Info

start page

  • 1543

end page

  • 8

volume

  • 98

number

  • 4