肿瘤转移是一个复杂的过程，有很多促癌基因基因参与其中过程。转移相关基因1（MTA1）是一个能调控多个靶蛋白的基因，该基因的表达有助于促进肿瘤转移过程。
MTA1表达已被证明与多种具有侵略性癌症类型密切相关包括乳腺癌。最新一项研究表明，MTA1能调控Smad7，SMAD7是转化生长因子β（TGFbeta）信号的一个组成部分。TGFbeta信号通过Smad蛋白家族转导到细胞核蛋白，其中就包括Smad7，Smad7是一个抑制SMAD蛋白的分子，起着负调节TGFbeta的作用。
降低MTA1的表达，Smad7的表达会增加。用组蛋白去乙酰酶抑制剂处理细胞后，Smad7的表达也增加。研究发现MTA1被招募至Smad7蛋白的启动子区域。
Smad7能抑制Smad2和Smad3的活化，该研究表明MTA1被抑制后，SMAD蛋白的表达水平就会水平下降，同时MTA被抑制后，Smad7的下游调控的一系列蛋白也会降低表达。可见MTA1的表达是调节TGFbeta信号的重要成分，而Smad7通过调节MTA1的表达可能有助于肿瘤的形成和转移。（生物谷：Bioon.com）
编译自：MTA1-mediated transcriptional repression of SMAD7 in breast cancer cell lines
doi:10.1016/j.ejca.2012.06.019
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MTA1-mediated transcriptional repression of SMAD7 in breast cancer cell lines
Shimul Salota, Rajiv Gudea
Metastasis is a complex process facilitated by the action of several genes. Metastasis associated 1 (MTA1) gene is one such gene which assists the process of metastasis by regulating several molecular targets. MTA1 acts as part of a nucleosome remodelling and histone deacetylation complex, which is involved in transcriptional regulation. Expression of MTA1 has been shown to be closely correlated with aggressiveness in several types of cancers, including breast cancer. In the present study we show that MTA1 regulates SMAD7, a component of Transforming growth factor beta (TGFbeta) signalling. TGFbeta signals are transduced to the nucleus by the Smad family of proteins, which includes Smad7, an inhibitory SMAD, which acts as a negative regulator of TGFbeta. On knockdown of MTA1, SMAD7 expression increases. Treating cells with a histone deacetylase inhibitor also increases SMAD7 expression. MTA1 is recruited to SMAD7 promoter region. SMAD7 inhibits activation of SMAD2 and SMAD3 and we show that the levels of these active SMAD proteins are decreased in cells expressing shRNA against MTA1. We further show that on MTA1 knockdown, the expression of downstream targets of SMAD7 is decreased. MTA1 thus appears to regulate a key inhibitor of TGFbeta signalling, SMAD7. By regulating molecules like SMAD7 MTA1 might assist the process of tumourigenesis and metastasis
