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Myc 相关锌指蛋白在恶性肿瘤中的作用。

Roles of Myc-associated zinc finger protein in malignant tumors.

机构信息

Department of Epidemiology and Statistics, School of Public Health, Guilin Medical University, Guilin, China.

出版信息

Asia Pac J Clin Oncol. 2022 Dec;18(6):506-514. doi: 10.1111/ajco.13748. Epub 2022 Jan 30.

DOI:10.1111/ajco.13748
PMID:35098656
Abstract

As an important transcription factor that is widely expressed in most tissues of the human body, Myc-associated zinc finger protein (MAZ) has been reported highly expressed in many malignant tumors and thought to be a promising therapeutic target for cancer treatment. In this review, we aim to offer a comprehensive understanding of MAZ regulation in malignant tumors. The carboxy terminal of MAZ protein contains six C2H2 zinc fingers, and its regulation of transcription is based on the interaction between the GC-rich DNA binding sites of target genes and its carboxy-terminal zinc finger motifs. MAZ protein has been found to activate or inhibit the transcriptional initiation process of many target genes, as well as play an important role in the transcriptional termination process of some target genes, so MAZ poses dual regulatory functions in the initiation and termination process of gene transcription. Through the transcriptional regulation of c-myc and Ras gene family, MAZ poses an important role in the occurrence and development of breast cancer, pancreatic cancer, prostate cancer, glioblastoma, neuroblastoma, and other malignant tumors. Our review shows a vital role of MAZ in many malignant tumors and provides novel insight for cancer diagnosis and treatment.

摘要

作为一种广泛表达于人体大多数组织的重要转录因子,Myc 相关锌指蛋白(MAZ)在许多恶性肿瘤中呈高表达,被认为是癌症治疗有前途的治疗靶点。在这篇综述中,我们旨在全面了解 MAZ 在恶性肿瘤中的调控作用。MAZ 蛋白的羧基末端含有六个 C2H2 锌指,其转录调控是基于靶基因的富含 GC 的 DNA 结合位点与其羧基末端锌指基序之间的相互作用。已经发现 MAZ 蛋白可以激活或抑制许多靶基因的转录起始过程,以及在一些靶基因的转录终止过程中发挥重要作用,因此 MAZ 在基因转录的起始和终止过程中具有双重调节功能。通过对 c-myc 和 Ras 基因家族的转录调控,MAZ 在乳腺癌、胰腺癌、前列腺癌、胶质母细胞瘤、神经母细胞瘤等恶性肿瘤的发生发展中起着重要作用。我们的综述表明 MAZ 在许多恶性肿瘤中具有重要作用,并为癌症的诊断和治疗提供了新的思路。

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1
Roles of Myc-associated zinc finger protein in malignant tumors.Myc 相关锌指蛋白在恶性肿瘤中的作用。
Asia Pac J Clin Oncol. 2022 Dec;18(6):506-514. doi: 10.1111/ajco.13748. Epub 2022 Jan 30.
2
MAZ, a zinc finger protein, binds to c-MYC and C2 gene sequences regulating transcriptional initiation and termination.MAZ是一种锌指蛋白,它与c-MYC和C2基因序列结合,调节转录起始和终止。
Proc Natl Acad Sci U S A. 1992 Aug 15;89(16):7452-6. doi: 10.1073/pnas.89.16.7452.
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Two consecutive zinc fingers in Sp1 and in MAZ are essential for interactions with cis-elements.Sp1和MAZ中两个连续的锌指对于与顺式元件的相互作用至关重要。
J Biol Chem. 2001 Aug 10;276(32):30429-34. doi: 10.1074/jbc.M103968200. Epub 2001 Jun 6.
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Dual function of MAZ mediated by FOXF2 in basal-like breast cancer: Promotion of proliferation and suppression of progression.FOXF2介导的MAZ在基底样乳腺癌中的双重作用:促进增殖并抑制进展。
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Transcriptional regulation by zinc-finger proteins Sp1 and MAZ involves interactions with the same cis-elements.锌指蛋白Sp1和MAZ的转录调控涉及与相同顺式元件的相互作用。
Int J Mol Med. 2003 May;11(5):547-53.
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Fetal Alz-50 clone 1 (FAC1) protein interacts with the Myc-associated zinc finger protein (ZF87/MAZ) and alters its transcriptional activity.胎儿阿尔茨海默病相关 50 克隆 1(FAC1)蛋白与 Myc 相关锌指蛋白(ZF87/MAZ)相互作用,并改变其转录活性。
Biochemistry. 2000 Mar 28;39(12):3206-15. doi: 10.1021/bi992211q.
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Transcriptional repression from the c-myc P2 promoter by the zinc finger protein ZF87/MAZ.锌指蛋白ZF87/MAZ对c-myc P2启动子的转录抑制作用
J Biol Chem. 1999 Jul 2;274(27):19498-506. doi: 10.1074/jbc.274.27.19498.
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The DNA-binding and transcriptional activities of MAZ, a myc-associated zinc finger protein, are regulated by casein kinase II.MAZ(一种与 myc 相关的锌指蛋白)的 DNA 结合和转录活性受酪蛋白激酶 II 调控。
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MYC associated zinc finger protein promotes the invasion and metastasis of hepatocellular carcinoma by inducing epithelial mesenchymal transition.MYC相关锌指蛋白通过诱导上皮-间质转化促进肝细胞癌的侵袭和转移。
Oncotarget. 2016 Dec 27;7(52):86420-86432. doi: 10.18632/oncotarget.13416.
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Interaction of Myc-associated zinc finger protein with DCC, the product of a tumor-suppressor gene, during the neural differentiation of P19 EC cells.在P19胚胎癌细胞的神经分化过程中,Myc相关锌指蛋白与肿瘤抑制基因产物DCC的相互作用。
Biochem Biophys Res Commun. 2001 Sep 7;286(5):1087-97. doi: 10.1006/bbrc.2001.5469.

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