STAT3 activation inhibits human bronchial epithelial cell apoptosis in response to cigarette smoke exposure

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

We have previously reported that cigarette smoke can induce DNA damage in human lung cells without leading to apoptosis or necrosis. In this study, we report that STAT3 is required for the survival of human bronchial epithelial cells (HBECs) following cigarette smoke-induced DNA damage. Cigarette smoke extract (CSE) exposure increases STAT3 phosphorylation (Tyr 705) and DNA binding activity in HBECs. CSE also stimulates IL-6 release and mRNA expression. Anti-IL-6 neutralizing antibody partially blocks STAT3 activation and renders the cells sensitive to CSE-induced DNA damage. Suppression of STAT3 by siRNA results in severe DNA damage and cell death in response to CSE exposure. These findings suggest that STAT3 mediates HBEC survival in response to CSE-induced DNA damage, at least in part, through the IL-6/STAT3 signaling pathway.

Original languageEnglish (US)
Pages (from-to)121-126
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume353
Issue number1
DOIs
StatePublished - Feb 2 2007

Fingerprint

Smoke
Tobacco Products
Epithelial Cells
Chemical activation
Apoptosis
DNA Damage
DNA
Interleukin-6
Phosphorylation
Cell death
Neutralizing Antibodies
Human Activities
Small Interfering RNA
Cell Survival
Cell Death
Necrosis
Lung
Messenger RNA

Keywords

  • Apoptosis
  • Cigarette smoke
  • STAT3

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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