Identification of a prostate-specific G-protein coupled receptor in prostate cancer

Xia, Chunzhi; Ma, Wenbin; Wang, Fen; Hua, Shao-bing; Liu, Mingyao

doi:10.1038/sj.onc.1204803

Cited by 80 publications

(62 citation statements)

References 35 publications

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“…AMACR has a key role in ␤-oxidation of dietary branched-chain fatty acids and is often overexpressed in PCs (23,24). OR51E2 is also overexpressed in PCs (25), but its function is unknown. RDOH functions in androgen catabolism and is likely to be associated with androgendependent prostate tumorigenesis.…”

Section: Molecular Features Of the Transition From Pins To Pcsmentioning

confidence: 99%

Molecular Features of the Transition from Prostatic Intraepithelial Neoplasia (PIN) to Prostate Cancer

et al. 2004

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To characterize the molecular feature in prostate carcinogenesis and the putative transition from prostatic intraepithelial neoplasia (PIN) to invasive prostate cancer (PC), we analyzed gene-expression profiles of 20 PCs and 10 high-grade PINs with a cDNA microarray representing 23,040 genes. Considering the histological heterogeneity of PCs and the minimal nature of PIN lesions, we applied laser microbeam microdissection to purify populations of PC and PIN cells, and then compared their expression profiles with those of corresponding normal prostatic epithelium also purified by laser microbeam microdissection. A hierarchical clustering analysis separated the PC group from the PIN group, except for three tumors that were morphologically defined as one very-high-grade PIN and two low-grade PCs, suggesting that PINs and PCs share some molecular features and supporting the hypothesis of PIN-to-PC transition. On the basis of this hypothesis, we identified 21 up-regulated genes and 63 down-regulated genes commonly in PINs and PCs compared with normal epithelium, which were considered to be involved in the presumably early stage of prostatic carcinogenesis. They included AMACR, OR51E2, RODH, and SMS. Furthermore, we identified 41 up-regulated genes and 98 down-regulated genes in the transition from PINs to PCs; those altered genes, such as POV1, CDKN2C, EPHA4, APOD, FASN, ITGB2, LAMB2, PLAU, and TIMP1, included elements that are likely to be involved in cell adhesion or the motility of invasive PC cells. The down-regulation of EPHA4 by small interfering RNA in PC cells lead to attenuation of PC cell viability. These data provide clues to the molecular mechanisms underlying prostatic carcinogenesis, and suggest candidate genes the products of which might serve as molecular targets for the prevention and treatment of PC.

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Section: Molecular Features Of the Transition From Pins To Pcsmentioning

confidence: 99%

Molecular Features of the Transition from Prostatic Intraepithelial Neoplasia (PIN) to Prostate Cancer

et al. 2004

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“…For example, MOR23 is expressed both in the olfactory epithelium and in sperm and functions as a chemosensing receptor during sperm-egg communication, thereby modulating fertilization in the reproductive system [38] . The new olfactory receptor family members PSGR1 and PSGR2 have been found to have restricted expression in human prostate tissues, as shown by Northern blot and real-time PCR analysis of over 20 different human tissue types [39][40][41] . PSGR subfamily expression increases significantly in the epithelial cells of prostate intraepithelial neoplasia (PIN) patients and in prostate cancer patients relative to non-cancerous controls and benign prostatic hyperplasia tissues, suggesting that the PSGR subfamily may play an important role in early prostate cancer development [42] .…”

Section: Psgrs Subfamily In Prostate Cancermentioning

confidence: 99%

Orphan G protein-coupled receptors (GPCRs): biological functions and potential drug targets

et al. 2012

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The superfamily of G protein-coupled receptors (GPCRs) includes at least 800 seven-transmembrane receptors that participate in diverse physiological and pathological functions. GPCRs are the most successful targets of modern medicine, and approximately 36% of marketed pharmaceuticals target human GPCRs. However, the endogenous ligands of more than 140 GPCRs remain unidentified, leaving the natural functions of those GPCRs in doubt. These are the so-called orphan GPCRs, a great source of drug targets. This review focuses on the signaling transduction pathways of the Adhesion GPCR family, the LGR subfamily, and the PSGR subfamily, and their potential functions in immunology, development, and cancers. In this review, we present the current approaches and difficulties of orphan GPCR deorphanization and characterization.

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“…Our evaluation of PSGR expression in 50 different normal human adult and fetal tissues showed the presence of PSGR mRNA only in human prostate tissue. 6 While independent reports have confirmed predominant expression of PSGR in human prostate, 8,9 in one study where specific regions of human brain were analyzed. PSGR expression was also noted in the olfactory zone and the medula oblongata.…”

Section: Introductionmentioning

confidence: 99%

Quantitative expression profile of PSGR in prostate cancer

Sun

Petrovics

et al. 2005

Prostate Cancer Prostatic Dis

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PSGR is a novel member of the G-protein-coupled olfactory receptor family. Our initial report showed predominant expression of the PSGR in human prostate gland and significant alterations of PSGR expression in primary prostate cancer (CaP) specimens. The aim of this study was to provide in-depth evaluations of the expression profile of PSGR in prostatic epithelial cells of CaP patients and to evaluate the association of PSGR expression characteristics with clinico-pathologic features. In total, 220 RNA specimens, from laser capture microdissected paired benign and malignant prostatic epithelial cells of 110 CaP patients, were analyzed for PSGR expression by quantitative real-time PCR. The differential expression of PSGR between the prostatic epithelial cells of malignant and benign glands was statistically significant (Po0.0001). Comparison of PSGR expression between paired benign and tumor cells revealed prostate tumor cell-specific overexpression in 67.2% of tumor specimens (74 of 110), decreased expression in 20.9% of tumor specimens (23 of 110) and no difference of PSGR expression between tumor and normal cells in 11.8% of specimens (13 of 110). In representative cases, PSGR expression patterns were independently confirmed by in situ RNA hybridization. The PSGR overexpression associated with higher percentage of pathologic stage, pT3, and a higher level of preoperative serum PSA. CaP cells of African-American CaP patients exhibited about two-fold increase of PSGR expression in comparison to the Caucasian American CaP patients. Strikingly high-percentage CaP cells overexpress PSGR warrants further studies of PSGR expression alterations to define subsets of CaPs.

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Identification of a prostate-specific G-protein coupled receptor in prostate cancer

Cited by 80 publications

References 35 publications

Molecular Features of the Transition from Prostatic Intraepithelial Neoplasia (PIN) to Prostate Cancer

Molecular Features of the Transition from Prostatic Intraepithelial Neoplasia (PIN) to Prostate Cancer

Orphan G protein-coupled receptors (GPCRs): biological functions and potential drug targets

Quantitative expression profile of PSGR in prostate cancer

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