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Ventral prostate predominant l , a novel mouse gene expressed exclusively in the prostate *
Author(s) -
Wubah Judith A.,
Fischer Carolyn M.,
Rolfzen Laura N.,
Khalili May,
Kang Jason,
Green Jeffrey E.,
Bieberich Charles J.
Publication year - 2002
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.10060
Subject(s) - prostate , tramp , prostate cancer , gene expression , biology , prostate diseases , gene , pca3 , androgen , messenger rna , endocrinology , medicine , genetics , cancer , hormone
BACKGROUND Despite the region‐specific nature of human prostate disease, there is a paucity of information regarding the molecular basis of prostate regionalization and patterning. To elucidate genetic mechanisms that underlie prostate growth and development, we investigated differential gene expression in mouse prostate lobes. METHODS mRNA differential display analysis was used to identify differentially expressed genes during development of ventral, anterior, and dorsolateral prostate lobes. Differential gene expression was confirmed by Northern blot analysis and RT‐PCR. RESULTS A novel gene, Ventral prostate predominant1 ( Vpp1 ) was identified. Vpp1 mRNA was evident in all lobes but accumulated predominantly in the ventral prostate, and was detected on postnatal day 7 through adulthood exclusively in the prostate gland. The steady‐state level of Vpp1 mRNA decreased markedly in response to castration, suggesting androgen regulation of Vpp1 expression. Analysis of TRAMP tumors demonstrated a dramatic decrease in the level of Vpp1 mRNA. CONCLUSIONS The spatial distribution and early postnatal onset of Vpp1 expression is consistent with a role for this gene in prostate regionalization. The absolute prostate specificity of Vpp1 expression may allow this gene to serve as a paradigm to study the molecular basis of gene expression that is restricted exclusively to the prostate gland. Prostate 51:21–29, 2002. © 2002 Wiley‐Liss, Inc.