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Nat Com：上海生科院胡国宏教授发现miR-182能抑制癌症转移

2016-12-23 佚名 生物谷

胡国宏
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2016年12月22日讯 /生物谷BIOON/ --近日，来自中科院上海生科院的胡国宏研究组在国际学术期刊Nature Communications上发表了一项新研究成果，他们在这篇文章中阐述了一种microRNA如何破坏细胞对TGFβ信号途径的自我调节，进而促进TGFβ信号途径介导的癌细胞转移。该研究为阻止肿瘤进展，遏制癌细胞转移提供了一个新靶点。该研究通讯作者为胡国宏研究员，第一作者为余静宜博


近日，来自中科院上海生科院的胡国宏研究组在国际学术期刊Nature Communications上发表了一项新研究成果，他们在这篇文章中阐述了一种microRNA如何破坏细胞对TGFβ信号途径的自我调节，进而促进TGFβ信号途径介导的癌细胞转移。该研究为阻止肿瘤进展，遏制癌细胞转移提供了一个新靶点。

该研究通讯作者为胡国宏研究员，第一作者为余静宜博士。

TGF信号途径在癌细胞发生上皮间充质转化（EMT）和转移的过程中发挥关键作用。SMAD7既是TGFβ信号途径的一个转录靶基因产物又是该途径的一个负调节因子，SMAD7介导了一个调节TGF信号途径的负反馈回路，利用这一点或可限制癌细胞对TGF信号的应答。

在这项最新研究中，研究人员发现利用TGFβ处理细胞能够诱导一些癌细胞内SMAD7的转录，但是并不能改变SMAD7的蛋白水平。为了找出原因，研究人员进行了机制研究，由于microRNA是进行这类转录后调节的一种机制，他们分析认为microRNA可能与SMAD7蛋白合成的调节有关。因此他们通过软件预测发现microRNA-182可能在这一过程中发挥了作用，通过进一步实验证明TGFβ能够激活microRNA-182（miR-182）的表达，而miR-182又会进一步抑制SMAD7的蛋白合成。

研究结果表明沉默miR-182会导致癌细胞在受到TGFβ处理后发生SMAD7的表达上调，进而阻止TGFβ诱导的EMT和癌细胞侵袭。而过表达miR-182则会促进乳腺肿瘤的侵袭以及骨转移过程中TGFβ诱导的破骨细胞生成。研究人员又进一步发现miR-182的表达与人类肿瘤样本中SMAD7的蛋白表达水平成负相关性。

这些研究结果表明miR-182能够破坏TGFβ信号途径的自我调节，该研究为解释转移性癌细胞对TGFβ信号途径的应答提供了一种可能机制，也为遏制癌细胞转移提供了一个新靶点。

原始出处

Jingyi Yu, Rong Lei, Xueqian Zhuang, Xiaoxun Li, Gang Li, Sima Lev, Miguel F. Segura, Xue Zhang & Guohong Hu.MicroRNA-182 targets SMAD7 to potentiate TGFβ-induced epithelial-mesenchymal transition and metastasis of cancer cells.Nat Com.2016

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    2017-01-16 木头人513

    #上海生科院#

    0

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    2017-08-10 liye789132251

    #Nat#

    0

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    2017-02-07 smallant2002

    #miR#

    0

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    2016-12-25 hb2008ye

    #癌症转移#

    0