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Updated: Jan 29, 2026
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Comparing the Effects of Electronic Cigarette Vapor and Cigarette Smoke in a Novel In Vivo Exposure System
Published on: May 24, 2017
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Cigarette smoking promotes bladder cancer via increased platelet-activating factor
Shannon Kispert1, John Marentette2, Jane McHowat3
1Department of Biology, University of North Georgia, Oakwood, Georgia.
Physiological Reports
|February 14, 2019
Summary
Cigarette smoke extract (CSE) increases Platelet Activating Factor (PAF) and its receptor (PAF-R) in bladder cancer cells, promoting tumor cell adhesion and metastasis. Targeting the PAF-PAFR pathway may offer a new therapeutic strategy for smokers with bladder cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Cigarette smoking is a primary risk factor for bladder cancer, linked to tumor growth and metastasis.
- Platelet-activating factor (PAF) and its receptor (PAF-R) mediate cell migration across the endothelium.
- The role of PAF-PAFR signaling in smoking-related bladder cancer progression is not fully understood.
Purpose of the Study:
- To investigate the effect of cigarette smoke extract (CSE) on PAF and PAF-R expression in bladder cancer.
- To determine if CSE influences bladder cancer cell adhesion to endothelial cells.
- To explore the potential of targeting the PAF-PAFR pathway in smoking-associated bladder cancer.
Main Methods:
- Exposure of bladder cancer cells to cigarette smoke extract (CSE).
- Measurement of PAF accumulation and PAF-R expression.
- Assessment of bladder cancer cell adherence to bladder endothelial cells, with and without ginkgolide B pretreatment.
- Immunohistochemical analysis of PAF and PAF-R in tumor biopsies from smokers.
Main Results:
- CSE exposure led to increased PAF accumulation and PAF-R expression in bladder cancer cells.
- CSE enhanced bladder cancer cell adherence to bladder endothelial cells.
- Ginkgolide B pretreatment abrogated CSE-induced cell adherence.
- Tumor tissues from smoking bladder cancer patients showed elevated PAF and PAF-R levels compared to normal tissue.
Conclusions:
- CSE influences the PAF-PAFR pathway in bladder cancer, potentially promoting tumor growth and metastasis.
- The PAF-PAFR interaction represents a potential therapeutic target for bladder cancer in smokers.
- Further research into targeting this pathway could lead to novel treatment strategies.
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