摘要
男性前列腺癌在发达国家中是非常普遍的,但检测癌症的显著比例保持惰性,没有成为强劲的癌。这凸显了需要改进可以区分懒惰的和有潜在危险的情况之间的生物标志物。前列腺特异性G蛋白偶联受体(PSGR 或者OR51E2)是一个在人类前列腺上皮细胞特异性高表达嗅觉受体家族成员,它高表达于PIN和前列腺癌。前列腺特异性G蛋白偶联受体已经参与了前列腺癌细胞的侵袭性,提示在转移性前列腺癌的转移的潜在作用。最近,转基因小鼠过度表达的前列腺特异性G蛋白偶联受体在前列腺报告制定急性炎症反应,其次是低级PIN出现,而前列腺特异性G蛋白偶联受体的小鼠过度表达PTEN的缺失具有侵袭性前列腺癌的小鼠加速形成。本文将总结最近的对前列腺特异性G蛋白偶联受作为一个潜在的前列腺癌生物标志物和前列腺癌的侵袭和炎症调节作用的焦点体的角色。
关键词: 肿瘤标志物,G蛋白偶联受体,炎症浸润,嗅觉受体,前列腺特异性G蛋白偶联受体,前列腺癌。
Current Molecular Medicine
Title:Prostate-Specific G-Protein Coupled Receptor, an Emerging Biomarker Regulating Inflammation and Prostate Cancer Invasion
Volume: 16 Issue: 6
Author(s): M. Rodriguez, S. Siwko, M. Liu
Affiliation:
关键词: 肿瘤标志物,G蛋白偶联受体,炎症浸润,嗅觉受体,前列腺特异性G蛋白偶联受体,前列腺癌。
摘要: Prostate cancer is highly prevalent among men in developed countries, but a significant proportion of detected cancers remain indolent, never progressing into aggressive carcinomas. This highlights the need to develop refined biomarkers that can distinguish between indolent and potentially dangerous cases. The prostate-specific G-protein coupled receptor (PSGR, or OR51E2) is an olfactory receptor family member with highly specific expression in human prostate epithelium that is highly overexpressed in PIN and prostate cancer. PSGR has been functionally implicated in prostate cancer cell invasiveness, suggesting a potential role in the transition to metastatic PCa. Recently, transgenic mice overexpressing PSGR in the prostate were reported to develop an acute inflammatory response followed by emergence of low grade PIN, whereas mice with compound PSGR overexpression and loss of PTEN exhibited accelerated formation of invasive prostate adenocarcinoma. This article will review recent PSGR findings with a focus on its role as a potential prostate cancer biomarker and regulator of prostate cancer invasion and inflammation.
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Cite this article as:
M. Rodriguez, S. Siwko, M. Liu , Prostate-Specific G-Protein Coupled Receptor, an Emerging Biomarker Regulating Inflammation and Prostate Cancer Invasion, Current Molecular Medicine 2016; 16 (6) . https://dx.doi.org/10.2174/1566524016666160607091333
DOI https://dx.doi.org/10.2174/1566524016666160607091333 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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