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COMPARATIVE STUDY
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Effects of cigarette smoke condensate on oral squamous cell carcinoma cells.
Archives of Oral Biology 2011 October
OBJECTIVE: Epidemiological studies have reported that tobacco use is a major etiological factor for oral cancer. Several matrix metalloproteinases (MMPs) have been shown to play important roles in the invasion and metastasis of oral squamous cell carcinomas, especially MMP-2 and MMP-9. This study examined the effects of cigarette smoke condensate (CSC) on oral cancer cells.
DESIGN: Two oral squamous cell carcinoma cell lines, SCC-25 (metastatic) and CAL-27 (non-metastatic), were exposed to different concentrations of CSC and examined for their collagen degrading ability and MMP production using collagen degradation assays, zymograms and Western blots.
RESULTS: Exposure to CSC increased the collagen degrading ability of the metastasizing cell line (SCC-25) by a mechanism involving increased MMP-2 and MMP-9 production.
CONCLUSION: CSC increased the collagen degrading ability of SCC-25 by increasing the MMP-2 and MMP-9 protein levels. Continued cigarette smoking in oral cancer patients may result in decreased survival rates due to enhanced metastatic potential of the cancer cells.
DESIGN: Two oral squamous cell carcinoma cell lines, SCC-25 (metastatic) and CAL-27 (non-metastatic), were exposed to different concentrations of CSC and examined for their collagen degrading ability and MMP production using collagen degradation assays, zymograms and Western blots.
RESULTS: Exposure to CSC increased the collagen degrading ability of the metastasizing cell line (SCC-25) by a mechanism involving increased MMP-2 and MMP-9 production.
CONCLUSION: CSC increased the collagen degrading ability of SCC-25 by increasing the MMP-2 and MMP-9 protein levels. Continued cigarette smoking in oral cancer patients may result in decreased survival rates due to enhanced metastatic potential of the cancer cells.
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