Cigarette smoke modulates PC3 prostate cancer cell migration by altering adhesion molecules and the extracellular matrix

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Cigarette smoke modulates PC3 prostate cancer cell migration by altering adhesion molecules and the extracellular matrix

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Title: Cigarette smoke modulates PC3 prostate cancer cell migration by altering adhesion molecules and the extracellular matrix
Author: YANG, SUPING; LONG, MINICA; TACHADO, SOUVENIR D.; SENG, SEYHA

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Citation: YANG, SUPING, MINICA LONG, SOUVENIR D. TACHADO, and SEYHA SENG. 2015. “Cigarette smoke modulates PC3 prostate cancer cell migration by altering adhesion molecules and the extracellular matrix.” Molecular Medicine Reports 12 (5): 6990-6996. doi:10.3892/mmr.2015.4302. http://dx.doi.org/10.3892/mmr.2015.4302.
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Abstract: Prostate cancer (PCa) is the second leading cause of cancer-related mortality among American males. Studies suggest that cigarette smoking is associated with the progression of PCa; however, the molecular mechanisms underlying this process have not been extensively investigated. PCa progression is characterized by increased cell migration and alterations in extracellular matrix (ECM)- and cell adhesion molecule (CAM)-related gene expression. In the present study, the influence of cigarette smoke medium (SM) on cell migration and on the expression of ECM- and CAM-related genes in PC3 prostate adenocarcinoma cells was investigated. According to a wound-healing assay, SM treatment promoted PC3 cell migration. RNA expression levels from SM-treated and control cells were analyzed using a polymerase chain reaction (PCR) array. Of 84 genes analyzed, 27.38% (23/84) exhibited a ≥2-fold change in threshold cycle in PC3 cells following 0.5% SM treatment. Functional gene grouping analysis demonstrated that SM treatment modulated the RNA transcription of approximately 18.4% of CAMs and 33.93% of ECM-related genes. Quantitative PCR analysis showed that SM treatment led to a significant decrease in transcription levels of the following genes: Collagen 5 α-1(V), connective tissue growth factor, integrin β-2, kallmann syndrome 1, laminin α 3, matrix metallopeptidase 7 (MMP7), MMP13, secreted protein acidic cysteine-rich, thrombospondin-2 and versican; and that SM significantly increased the transcription levels of MMP2 and MMP12. Furthermore, MMP2 knockdown significantly reduced the migration of SM-treated PC3 cells. The present study provides novel insights into the association of cigarette smoking with PCa progression, via the alteration of ECM/CAM interactions.
Published Version: doi:10.3892/mmr.2015.4302
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4626126/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:25658403
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