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三联基序蛋白59的下调抑制乳腺癌细胞的增殖、迁移和侵袭。

Down-regulation of tripartite motif protein 59 inhibits proliferation, migration and invasion in breast cancer cells.

作者信息

Zhang Yan, Yang Wen-Bin

机构信息

Department of General Surgery, The Second Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an 710004, China.

Department of General Surgery, The Second Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an 710004, China.

出版信息

Biomed Pharmacother. 2017 May;89:462-467. doi: 10.1016/j.biopha.2017.02.039. Epub 2017 Feb 27.

DOI:10.1016/j.biopha.2017.02.039
PMID:28249247
Abstract

Tripartite motif protein 59 (TRIM59), also known as mouse ring finger protein 1 (MRF1), is a surface molecule and belongs to the TRIM family. Recently, TRIM59 has been described in multiple cancers such as gastric, prostatic and lung cancer. However, there have been no reports on its functions in breast cancer. In this study, we elucidated the biological roles of TRIM59 in breast cancer. We found that TRIM59 was up-regulated in breast cancer cells. Down-regulation of TRIM59 inhibited breast cancer cell proliferation, migration and invasion in vitro as well as tumor growth in vivo. In addition, TRIM59 down-regulation reduced the protein expression level of p-Smad2 and thus inhibited the activity of transforming growth factor-β (TGF-β) signaling. Taken together, our study results provided new evidence showing that TRIM59 may be considered as a promising therapeutic target for breast cancer.

摘要

三聚体基序蛋白59(TRIM59),也被称为小鼠环指蛋白1(MRF1),是一种表面分子,属于TRIM家族。最近,TRIM59已在多种癌症中被描述,如胃癌、前列腺癌和肺癌。然而,关于其在乳腺癌中的功能尚无报道。在本研究中,我们阐明了TRIM59在乳腺癌中的生物学作用。我们发现TRIM59在乳腺癌细胞中上调。TRIM59的下调在体外抑制乳腺癌细胞的增殖、迁移和侵袭以及体内肿瘤生长。此外,TRIM59的下调降低了p-Smad2的蛋白表达水平,从而抑制了转化生长因子-β(TGF-β)信号通路的活性。综上所述,我们的研究结果提供了新的证据,表明TRIM59可能被视为乳腺癌的一个有前景的治疗靶点。

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Down-regulation of tripartite motif protein 59 inhibits proliferation, migration and invasion in breast cancer cells.三联基序蛋白59的下调抑制乳腺癌细胞的增殖、迁移和侵袭。
Biomed Pharmacother. 2017 May;89:462-467. doi: 10.1016/j.biopha.2017.02.039. Epub 2017 Feb 27.
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