Nature Science关注癌症新突破

　　生物通报道，最新一期的著名杂志Nature刊发了一篇前列腺癌最新分子标记的文章，该研究成果为快速检测前列腺癌提供了新线索。今日Nature 和Science分别以头条新闻介绍了该研究成果。

　　

生物通报道，最新一期的著名杂志Nature刊发了一篇前列腺癌最新分子标记的文章，该研究成果为快速检测前列腺癌提供了新线索。今日Nature 和Science分别以头条新闻介绍了该研究成果。

 

一直以来，临床肿瘤医生们在前列腺癌的诊治过程中备受打击，他们往往能轻易地诊断出前列腺癌患者，却无法诊断出该患者是恶性前列腺癌还是良性前列腺癌，这往往导致恶性前列腺癌患者丧失了最佳治疗的机会。而美国密歇根大学这项新的研究成果有助临床肿瘤医生走出这个困境。

 

这一项目是密歇根大学，霍华休斯医学院的研究者最新的研究成果。研究者对前列腺癌样品中的代谢物所做的一项系统分析，他们发现一个问题：肌氨酸（包括肌肉在内的很多生物组织中的一种常见氨基酸）在侵略性前列腺癌中含量显著升高。

 

值得关注的是，肌氨酸在男性前列腺癌患者的尿样中可检测出来。这一发现使得肌氨酸成为前列腺癌诊断的一个候选生物标记。

 

更令人振奋的是，用遗传技术将甘氨酸生成肌氨酸的酶定向剔除，小鼠动物实验发现，剔除了生成肌氨酸的酶将大大降低前列腺癌的恶性程度，这说明肌氨酸在癌细胞转移中可能扮演重要角色，因此肌氨酸通道可能成为前列腺癌的新治疗靶位。（生物通 小茜）

 

Nature新闻页面：http://www.nature.com/news/2009/090211/full/news.2009.94.html

Science新闻页面：http://sciencenow.sciencemag.org/cgi/content/full/2009/211/1

 

生物通推荐原文摘要：Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression

【Abstract】

Multiple, complex molecular events characterize cancer development and progression1, 2. Deciphering the molecular networks that distinguish organ-confined disease from metastatic disease may lead to the identification of critical biomarkers for cancer invasion and disease aggressiveness. Although gene and protein expression have been extensively profiled in human tumours, little is known about the global metabolomic alterations that characterize neoplastic progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we profiled more than 1,126 metabolites across 262 clinical samples related to prostate cancer (42 tissues and 110 each of urine and plasma). These unbiased metabolomic profiles were able to distinguish benign prostate, clinically localized prostate cancer and metastatic disease. Sarcosine, an N-methyl derivative of the amino acid glycine, was identified as a differential metabolite that was highly increased during prostate cancer progression to metastasis and can be detected non-invasively in urine. Sarcosine levels were also increased in invasive prostate cancer cell lines relative to benign prostate epithelial cells. Knockdown of glycine-N-methyl transferase, the enzyme that generates sarcosine from glycine, attenuated prostate cancer invasion. Addition of exogenous sarcosine or knockdown of the enzyme that leads to sarcosine degradation, sarcosine dehydrogenase, induced an invasive phenotype in benign prostate epithelial cells. Androgen receptor and the ERG gene fusion product coordinately regulate components of the sarcosine pathway. Here, by profiling the metabolomic alterations of prostate cancer progression, we reveal sarcosine as a potentially important metabolic intermediary of cancer cell invasion and aggressivity.（生物通）