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Nature Communications:解析抑癌基因

2013-03-11 生物通 生物通

从1979年发现至今,p53已经历经30多年的岁月,关于p53的文章层出不穷,每当我们觉得离p53的真相接近之时才发现,p53仍是我们最熟悉的陌生人。这个明星抑癌基因至今已被发现与多种作用因子,信号途径有关,近期来自中国科技大学,美国滨州大学医学院等处的研究人员就发现了一种抑癌基因读码框移位蛋白(Alternative reading frame protein,ARF)相关酶Siva1与p53在

从1979年发现至今,p53已经历经30多年的岁月,关于p53的文章层出不穷,每当我们觉得离p53的真相接近之时才发现,p53仍是我们最熟悉的陌生人。这个明星抑癌基因至今已被发现与多种作用因子,信号途径有关,近期来自中国科技大学,美国滨州大学医学院等处的研究人员就发现了一种抑癌基因读码框移位蛋白(Alternative reading frame protein,ARF)相关酶Siva1与p53在癌症发生发展过程中的作用机制,相关成果公布在《自然—通讯》(Nature Communications)杂志上。

文章的通讯作者分别是中国科技大学生命科学学院吴缅教授,以及梅一德教授,这两位学者都是知名的癌症研究人员,前者聚焦于p53与肿瘤代谢;非编码RNA与肿瘤;ips分子调控机制等方面的研究,后者主要从事原癌基因和肿瘤抑制基因相互作用,以及其在肿瘤形成中的功能等方面的研究。

抑癌基因读码框移位蛋白(tumour suppressor alternative reading frame)是人类癌症发生过程中最长久的突变蛋白之一,之前的研究证明,ARF能通过直接抑制Mdm2,稳定和激活p53。这种对于致癌应激的应答反应,被认为是针对癌症的一种重要保护性决定因素。

然而关于细胞内的ARF调控,至今科学家们了解的并不多,为此在这篇文章中,研究人员展开了深入探讨,发现了一种特异性ARF的E3泛素连接酶Siva1的关键作用机制。

研究人员发现Siva1在体内和体外都能与ARF相互作用,这种蛋白能通过直接相互作用,促进ARF的泛素化和降解,从而影响p53的稳定性。从功能上说,Siva1还能以ARF/p53依赖性的方式调节细胞周期进程和细胞增殖。

这些研究结果指出了ARF稳定性调控的一个新监控机制,揭示出了Siva1一个重要的功能:调控ARF-MDM2-p53通路。

2011年,这一研究组还曾发表了关于Siva1蛋白的研究发现:Siva1蛋白在上皮细胞-间质细胞的转化(EMT)和肿瘤转移的调控中发挥着重要作用。寻找控制肿瘤转移的关键分子及其致病机理,是目前开发新的抗癌药物的主要方式。这项研究工作表明,Siva1可以作为一个潜在的抑制肿瘤转移的治疗靶点,应用于抗肿瘤药物的研发;并且Siva1和pS16-Stathmin的水平可以作为乳腺癌恶性程度的标记,应用于临床上乳腺癌的早期诊断。

抑癌相关的拓展阅读:

doi:10.1038/ncomms2533 
PMC:
PMID:

Siva1 inhibits p53 function by acting as an ARF E3 ubiquitin ligase

Xingwu Wang, Meng Zha, Xiaocheng Zhao, Peng Jiang, Wenjing Du, Mian Wu

The tumour suppressor alternative reading frame (ARF) is one of the most frequently mutated proteins in human cancer. It has been well established that ARF is able to stabilize and activate p53 by directly inhibiting Mdm2. ARF-mediated p53 activation in response to oncogenic stress is thought to be an important determinant of protection against cancer. However, little is known regarding the control of ARF in cells. Here, we show that Siva1 is a specific E3 ubiquitin ligase of ARF. Siva1 physically interacts with ARF both in vitro and in vivo. Through direct interaction, Siva1 promotes the ubiquitination and degradation of ARF, which in turn affects the stability of p53. Functionally, Siva1 regulates cell cycle progression and cell proliferation in an ARF/p53-dependent manner. Our results uncover a novel regulatory mechanism for the control of ARF stability, thereby revealing an important function of Siva1 in the regulation of the ARF-Mdm2-p53 pathway.

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    2013-06-25 liuli5079
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    2013-10-30 hongbochen
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    2013-11-21 liye789132251
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