STAT3 activation inhibits human bronchial epithelial cell apoptosis in response to cigarette smoke exposure
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.
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Cigarette smoke extract induces IL-6 expression and increases levels of pY-STAT3 and STAT3-DNA binding in human bronchial epithelial cells, which protects these cells from apoptosis.
“Cigarette smoke extract (CSE) induced IL-6 expression and increased levels of pY-STAT3 and STAT3-DNA binding in human bronchial epithelial cells (HBECs) (Liu, 2007), which protected these cells from apoptosis.”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Liu, 2007
Anti-IL-6 neutralizing antibody and STAT3 siRNA render HBECs sensitive to CSE-induced DNA damage, suggesting that STAT3 mediates HBEC survival in response to CSE-induced DNA damage.
“Anti–IL-6 neutralizing antibody, as well as STAT3 small interfering RNA (siRNA), rendered HBECs sensitive to CSE-induced DNA damage, suggesting that STAT3 mediates HBEC survival in response to CSE-induced DNA damage (Liu, 2007).”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Liu, 2007
Cites
Bowman, T., Garcia, R., Turkson, J., & Jove, R. (2000) · Oncogene · doi:10.1038/sj.onc.1203527 · Cited by 1,743 · see citing works
Takeda, K., Kaisho, T., Yoshida, N., Takeda, J., Kishimoto, T., & Akira, S. (1998) · The Journal of Immunology · doi:10.4049/jimmunol.161.9.4652 · Cited by 584 · see citing works
Th2 cytokine regulation of type I collagen gel contraction mediated by human lung mesenchymal cells
Liu, X., Kohyama, T., Wang, H., Zhu, Y. K., Wen, F.-Q., Kim, H. J., Romberger, D. J., & Rennard, S. I. (2002) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00321.2001 · Cited by 77 · see citing works
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Bharadwaj, U., Kasembeli, M. M., Robinson, P., & Tweardy, D. J. (2020) · Pharmacological Reviews · doi:10.1124/pr.119.018440 · Cited by 314 · see citing works
“Anti–IL-6 neutralizing antibody, aswell as STAT3 small interfering RNA (siRNA), rendered HBECs sensitive to CSE-induced DNA damage, suggesting that STAT3 mediates HBEC survival in response to CSE-induced DNA damage (Liu, 2007).”
Background
- Authors
- Liu, X.
- Affiliations
- University of Nebraska Medical Center (US)
- Corresponding author
- Liu, Xiangde
- ORCID
- Liu, Xiangde
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2007-02
- Volume
- 353
- Issue
- 1
- Pages
- 121-126
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W2050660882
- Cited by
- 33
- References
- 3
- Citations by year
- 2026: 1 · 2025: 1 · 2022: 1 · 2021: 1 · 2020: 5 · 2017: 2 · 2016: 1 · 2015: 2 · 2014: 2 · 2012: 2
- FWCI
- 1.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Biochemical and Biophysical Research Communications (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- STAT3 activation, cigarette smoke extract, human bronchial epithelial cells, apoptosis, DNA damage, interleukin-6, STAT3 phosphorylation, cell survival, IL-6/STAT3 signaling pathway, siRNA knockdown
- MeSH terms
- Bronchi, Cell Line, Cells, Cultured, Dose-Response Relationship, Drug, Epithelial Cells, Humans, Tars, Tobacco Smoke Pollution, Apoptosis, STAT3 Transcription Factor
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