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Tumor suppressor function of PGP9.5 is associated with epigenetic regulation in prostate cancer--novel predictor of biochemical recurrence after radical surgery.

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Tumor suppressor function of PGP9.5 is associated with epigenetic regulation in prostate cancer--novel predictor of biochemical recurrence after radical surgery.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mitsui, Yozo Shiina, Hiroaki Hiraki, Miho Arichi, Naoko Hiraoka, Takeo Sumura, Masahiro Honda, Satoshi Yasumoto, Hiroaki Igawa, Mikio
Description	Country affiliation: Japan Author Affiliation: Mitsui Y ( Department of Urology, Shimane University School of Medicine, Izumo, Shimane, Japan.)
Abstract	BACKGROUND: The expression level of protein G product 9.5 (PGP9.5) is downregulated because of promoter CpG hypermethylation in several tumors. We speculated that impaired regulation of PGP9.5 through epigenetic pathways is associated with the pathogenesis of prostate cancer. METHODS: CpG methylation of the PGP9.5 gene was analyzed in cultured prostate cancer cell lines, 226 localized prostate cancer samples from radical prostatectomy cases, and 80 benign prostate hyperplasia (BPH) tissues. RESULTS: Following 5-aza-2'-deoxycytidune treatment, increased PGP9.5 mRNA transcript expression was found in the LNCaP and PC3 cell lines. With bisulfite DNA sequencing, partial methylation of the PGP9.5 promoter was shown in LNCaP whereas complete methylation was found in PC3 cells. After transfection of PGP9.5 siRNA, cell viability was significantly accelerated in LNCaP but not in PC3 cells as compared with control siRNA transfection. Promoter methylation of PGP9.5 was extremely low in only one of 80 BPH tissues, whereas it was found in 37 of 226 prostate cancer tissues. Expression of the mRNA transcript of PGP9.5 was significantly lower in methylation (+) than methylation (-) prostate cancer tissues. Multivariate analysis of biochemical recurrence (BCR) after an radical prostatectomy revealed pT category and PGP9.5 methylation as prognostically relevant. Further stratification with the pT category in addition to methylation status identified a stepwise reduction of BCR-free probability. CONCLUSION: This is the first clinical and comprehensive study of inactivation of the PGP9.5 gene via epigenetic pathways in primary prostate cancer. IMPACT: CpG methylation of PGP9.5 in primary prostate cancer might become useful as a molecular marker for early clinical prediction of BCR after radical prostatectomy.
File Format	HTM / HTML
ISSN	10559965
e-ISSN	15387755
Journal	Cancer Epidemiology Biomarkers & Prevention
Issue Number	3
Volume Number	21
Language	English
Publisher	American Association for Cancer Research
Publisher Date	2012-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cancer epidemiology Dna Methylation Epigenomics Gene Expression Regulation, Neoplastic Neoplasm Recurrence, Local Genetics Prostatectomy Prostatic Neoplasms Ubiquitin Thiolesterase Apoptosis Blotting, Western Cell Proliferation Cpg Islands Dna, Neoplasm Immunoenzyme Techniques Metabolism Surgery Promoter Regions, Genetic Prostatic Hyperplasia Rna, Small Interfering Real-time Polymerase Chain Reaction Tumor Cells, Cultured Antagonists & Inhibitors
Content Type	Text
Resource Type	Article
Subject	Epidemiology Oncology

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Tumor suppressor function of PGP9.5 is associated with epigenetic regulation in prostate cancer--novel predictor of biochemical recurrence after radical surgery.