Overexpression, amplification, and androgen regulation of TPD52 in prostate cancer.

TitleOverexpression, amplification, and androgen regulation of TPD52 in prostate cancer.
Publication TypeJournal Article
Year of Publication2004
AuthorsRubin MA, Varambally S, Beroukhim R, Tomlins SA, Rhodes DR, Paris PL, Hofer MD, Storz-Schweizer M, Kuefer R, Fletcher JA, Hsi B-L, Byrne JA, Pienta KJ, Collins C, Sellers WR, Chinnaiyan AM
JournalCancer Res
Volume64
Issue11
Pagination3814-22
Date Published2004 Jun 1
ISSN0008-5472
KeywordsAdult, Aged, Aged, 80 and over, Androgens, Chromosomes, Human, Pair 8, Gene Amplification, Gene Expression Regulation, Neoplastic, Humans, Immunohistochemistry, In Situ Hybridization, Fluorescence, Male, Middle Aged, Neoplasm Proteins, Nucleic Acid Hybridization, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, Prostatic Neoplasms
Abstract

Gains in the long arm of chromosome 8 (8q) are believed to be associated with poor outcome and the development of hormone-refractory prostate cancer. Based on a meta-analysis of gene expression microarray data from multiple prostate cancer studies (D. R. Rhodes et al., Cancer Res 2002;62:4427-33), a candidate oncogene, Tumor Protein D52 (TPD52), was identified in the 8q21 amplicon. TPD52 is a coiled-coil motif-bearing protein, potentially involved in vesicle trafficking. Both mRNA and protein levels of TPD52 were highly elevated in prostate cancer tissues. Array comparative genomic hybridization and amplification analysis using single nucleotide polymorphism arrays demonstrated increased DNA copy number in the region encompassing TPD52. Fluorescence in situ hybridization on tissue microarrays confirmed TPD52 amplification in prostate cancer epithelia. Furthermore, our studies suggest that TPD52 protein levels may be regulated by androgens, consistent with the presence of androgen response elements in the upstream promoter of TPD52. In summary, these findings suggest that dysregulation of TPD52 by genomic amplification and androgen induction may play a role in prostate cancer progression.

DOI10.1158/0008-5472.CAN-03-3881
Alternate JournalCancer Res.
PubMed ID15172988
Grant ListCA 97063 / CA / NCI NIH HHS / United States
P50CA69568 / CA / NCI NIH HHS / United States
P50CA90381 / CA / NCI NIH HHS / United States
R01AG21404 / AG / NIA NIH HHS / United States
T32 CA009172 / CA / NCI NIH HHS / United States