dc.contributor.author | YANG, SUPING | en_US |
dc.contributor.author | LONG, MINICA | en_US |
dc.contributor.author | TACHADO, SOUVENIR D. | en_US |
dc.contributor.author | SENG, SEYHA | en_US |
dc.date.accessioned | 2016-03-01T19:49:18Z | |
dc.date.issued | 2015 | en_US |
dc.identifier.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. | en |
dc.identifier.issn | 1791-2997 | en |
dc.identifier.uri | http://nrs.harvard.edu/urn-3:HUL.InstRepos:25658403 | |
dc.description.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. | en |
dc.language.iso | en_US | en |
dc.publisher | D.A. Spandidos | en |
dc.relation.isversionof | doi:10.3892/mmr.2015.4302 | en |
dc.relation.hasversion | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4626126/pdf/ | en |
dash.license | LAA | en_US |
dc.subject | cigarette smoke | en |
dc.subject | cell migration | en |
dc.subject | cell adhesion molecules | en |
dc.subject | extracellular matrix | en |
dc.subject | prostate cancer | en |
dc.title | Cigarette smoke modulates PC3 prostate cancer cell migration by altering adhesion molecules and the extracellular matrix | en |
dc.type | Journal Article | en_US |
dc.description.version | Version of Record | en |
dc.relation.journal | Molecular Medicine Reports | en |
dash.depositing.author | TACHADO, SOUVENIR D. | en_US |
dc.date.available | 2016-03-01T19:49:18Z | |
dc.identifier.doi | 10.3892/mmr.2015.4302 | * |
dash.contributor.affiliated | Tachado, Souvenir | |