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锌指蛋白121（ZNF121）与锌指BRK1结构域蛋白1（ZBRK1）和乳腺癌1号基因（BRCA1）相互作用，以调控它们在乳腺上皮细胞中的靶基因。

ZNF121 interacts with ZBRK1 and BRCA1 to regulate their target genes in mammary epithelial cells.

作者信息

Luo Ang, Zhang Kailun, Zhao Yanxia, Zhu Zhengmao, Fu Liya, Dong Jin-Tang

机构信息

Department of Genetics and Cell Biology Nankai University College of Life Sciences Tianjin China.

Present address: Department of Biochemistry, Molecular Biology and Biophysics University of Minnesota-Twin Cities 420 Washington Avenue SE Minneapolis MN 55455 USA.

出版信息

FEBS Open Bio. 2018 Nov 8;8(12):1943-1952. doi: 10.1002/2211-5463.12530. eCollection 2018 Dec.

DOI:10.1002/2211-5463.12530
PMID:30524945
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6275281/
Abstract

The novel zinc finger protein 121 (ZNF121) has been demonstrated to physically and functionally associate with the MYC oncoprotein to regulate cell proliferation and likely breast cancer development. To further understand how ZNF121 functions in cell proliferation and carcinogenesis, we identified and characterized the interaction of ZNF121 with zinc finger and BRCA1-interacting protein with a KRAB domain 1 (ZBRK1), a breast and ovarian cancer susceptibility protein 1 (BRCA1)-interacting protein, using the yeast two-hybrid assay and other approaches. We also found that ZNF121 bound to BRCA1. Functionally, ZFN121 suppressed the expression of ANG1 and HMGA2, two common downstream targets of ZBRK1 and BRCA1. Interestingly, ZNF121 also regulated the expression of BRCA1 and ZBRK1. These findings suggest that ZNF121 is likely a member of the BRCA1/CtIP/ZBRK1 repressor complex that plays a role in breast cancer.

摘要

新型锌指蛋白121（ZNF121）已被证明在物理和功能上与MYC癌蛋白相关联，以调节细胞增殖并可能参与乳腺癌的发展。为了进一步了解ZNF121在细胞增殖和致癌过程中的作用机制，我们利用酵母双杂交试验和其他方法，鉴定并表征了ZNF121与锌指和具有KRAB结构域的BRCA1相互作用蛋白1（ZBRK1，一种乳腺癌和卵巢癌易感蛋白1（BRCA1）相互作用蛋白）之间的相互作用。我们还发现ZNF121与BRCA1结合。在功能上，ZFN121抑制了ANG1和HMGA2的表达，这两个是ZBRK1和BRCA1共同的下游靶点。有趣的是，ZNF121还调节BRCA1和ZBRK1的表达。这些发现表明，ZNF121可能是BRCA1/CtIP/ZBRK1阻遏复合物的成员，在乳腺癌中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/9dc2d6dd4ab6/FEB4-8-1943-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/09174b461a06/FEB4-8-1943-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/1bd514f62bf4/FEB4-8-1943-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/5c8608fb0742/FEB4-8-1943-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/9dc2d6dd4ab6/FEB4-8-1943-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/09174b461a06/FEB4-8-1943-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/1bd514f62bf4/FEB4-8-1943-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/5c8608fb0742/FEB4-8-1943-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a685/6275281/9dc2d6dd4ab6/FEB4-8-1943-g004.jpg

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本文引用的文献

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ZBRK1, a novel tumor suppressor, activates VHL gene transcription through formation of a complex with VHL and p300 in renal cancer.ZBRK1是一种新型肿瘤抑制因子，在肾癌中通过与VHL和p300形成复合物来激活VHL基因转录。
Oncotarget. 2015 Mar 30;6(9):6959-76. doi: 10.18632/oncotarget.3134.
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Interruption of KLF5 acetylation converts its function from tumor suppressor to tumor promoter in prostate cancer cells.
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