HMG：雄激素调控miR-27a可能成为前列腺癌治疗新靶点

2012-07-10 Claire Fletcher 《人类分子遗传学》

英国伦敦帝国理工学院研究人员最新发现一个名为miR-27a的分子，其在促使前列腺癌症肿瘤生长过程中扮演着重要角色，未来可能成为前列腺癌症治疗的一个新靶点。前列腺癌是发生于男性前列腺组织中的恶性肿瘤。在欧美，它是男性最常患的癌症之一，仅在英国，每年就有大约36000人被诊断出患上该种疾病。前列腺癌的确切病因至今尚未明确，据信如基因和饮食等多种因素与其有关。而前列腺癌症肿瘤的生长则与雄性激素有关，雄

英国伦敦帝国理工学院研究人员最新发现一个名为miR-27a的分子，其在促使前列腺癌症肿瘤生长过程中扮演着重要角色，未来可能成为前列腺癌症治疗的一个新靶点。

前列腺癌是发生于男性前列腺组织中的恶性肿瘤。在欧美，它是男性最常患的癌症之一，仅在英国，每年就有大约36000人被诊断出患上该种疾病。前列腺癌的确切病因至今尚未明确，据信如基因和饮食等多种因素与其有关。而前列腺癌症肿瘤的生长则与雄性激素有关，雄性激素会刺激癌细胞分裂，进而促使肿瘤生长。

伦敦帝国理工学院研究人员在实验中发现，雄性激素会增加前列腺癌细胞中一种名为miR-27a的分子的数量，而这种分子对癌细胞生长具有极大的刺激作用，抑制这种分子，会使得前列腺癌细胞的生长速率降低一半。这表明，miR-27a这种分子极有可能成为前列腺癌症治疗的一个新靶点。

miR-27a属于微核糖核酸（microRNA）。微核糖核酸在调节基因活动方面具有重要作用，相比于蛋白质，微核糖核酸更易设计，也更易合成可轻易进入细胞内部的抑制分子，因而作为一个新的治疗靶点，科学家们对其更加看好。

这一研究成果发表在《人类分子遗传学》杂志上。论文第一作者、帝国理工学院的克莱尔·弗莱彻表示，新研究表明，miR-27a是雄性激素与前列腺肿瘤两者间的一个重要媒介，有可能成为前列腺治疗新方法的靶点。目前已经证明，在实验室中，抑制miR-27a分子就可以抑制前列腺肿瘤的生长，但这只是研究的第一步，未来还有许多障碍需要克服。他们下一步研究目标是要通过动物实验来对研究成果进行进一步验证，而要开发出适用于人类的新疗法，则至少还需要几年的时间

原始文献:

Fletcher CE, Dart DA, Sita-Lumsden A, Cheng H, Rennie PS, Bevan CL.

Androgen-regulated processing of the oncomir MiR-27a, which targets Prohibitin in prostate cancer.Hum Mol Genet. 2012 Jul 15;21(14):3112-27.

MicroRNAs (miRs) play an important role in the development of many complex human diseases and may have tumour suppressor or oncogenic (oncomir) properties. Prostate cancer is initially an androgen-driven disease, and androgen receptor (AR) remains a key driver of growth even in castration-resistant tumours. However, AR-mediated oncomiR pathways remain to be elucidated. We demonstrate that miR-27a is an androgen-regulated oncomir in prostate cancer, acting via targeting the tumour suppressor and AR corepressor, Prohibitin (PHB). Increasing miR-27a expression results in reduced PHB mRNA and protein levels, and increased expression of AR target genes and prostate cancer cell growth. This involves a novel mechanism for androgen-mediated miR regulation, whereby AR induces a transient increase in miR-23a27a24-2 transcription, but more significantly accelerates processing of the primiR-23a27a24-2 cluster. Androgens therefore regulate miR-27a expression both transcriptionally (via AR binding to the cluster promoter) and post-transcriptionally (accelerating primiR processing to the mature form). We further show that a miR-27a anti-sense oligonucleotide, by opposing the effects of mir-27a, has therapeutic potential in prostate cancer.

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2016-03-18 忠诚向上

好好学习

115 0
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2016-03-18 忠诚向上

好好学习

128 0
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2016-03-18 忠诚向上

好好学习

68 0
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2016-03-18 忠诚向上

好好学习

93 0
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2016-03-18 忠诚向上

好好学习

114 0
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2016-03-18 忠诚向上

好好学习

161 0
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2016-03-18 忠诚向上

好好学习

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