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Is cigarette smoking an independent risk factor of metastatic disease in prostate cancer? (1047.15)
Author(s) -
McHowat Jane,
Kispert Shan,
Marentette John,
Powell Jordan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1047.15
Subject(s) - platelet activating factor , prostate cancer , metastasis , lung cancer , medicine , cancer research , cancer , cancer cell , receptor , endothelium , risk factor , pharmacology
Cigarette smoking is a major risk factor in many health conditions, including cancer. Platelet‐activating factor (PAF) may contribute to cancer metastasis by increasing adherence of tumor cells to activated endothelium via the PAF‐PAF receptor interaction. We exposed PC‐3 prostate cancer cells to cigarette smoke extract (CSE) and measured PAH acetylhydrolase activity (PAF‐AH, inactivates PAF), PAF accumulation, PAF receptor expression and adherence to human lung microvascular endothelial cells (HMVEC‐L). CSE incubation (20 μg/ml, 4‐24 hours) resulted in a significant inhibition of PAF‐AH activity, and increased PAF accumulation in PC‐3 cells. Incubation of PC‐3 cells with CSE resulted in a 5‐fold increase in PAF receptor expression on the cell surface and increased adherence to HMVEC‐L. Pretreatment of PC‐3 cells with Ginkgolide B blocked adherence to the endothelium. Our data demonstrate that prostate cancer patients who smoke may be at increased risk for metastasis and that the nutraceutical Ginkgo biloba may be an adjunctive therapy to manage this disease.

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