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[SETD7在肿瘤发生发展中的作用及机制研究进展]

[Research Progress of Role and Mechanism of SETD7 in Tumor Occurrence 
and Progression].

作者信息

Cao Limin, Wang Min, Xu Ke

机构信息

Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, 
Tianjin Medical University General Hospital, Tianjin 300052, China.

出版信息

Zhongguo Fei Ai Za Zhi. 2023 Jan 20;26(1):38-45. doi: 10.3779/j.issn.1009-3419.2023.106.02.

DOI:10.3779/j.issn.1009-3419.2023.106.02
PMID:36792079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9987127/
Abstract

The occurence and development of tumors is a complicated process, which not only depends on the mutation or deletion of genes, but also is affected by epigenetic regulation. Accumulating evidences have shown that epigenetic modifications play fundamental roles in transcriptional regulation, heterochromatin formation, X chromosome inactivation, DNA damage response and tumor development. SET domain containing lysine methyltransferase 7 (SETD7) was initially identified as an important lysine methyltransferase, which methylated histone and non-histone proteins. These modifications play fundamental roles. Once this modification disorders, it can directly lead to cell abnormalities and cause many diseases. Studies have shown that SETD7 is related to the occurence and development of various tumors, but the methylation sites of SETD7 and its regulatory mechanism have not been fully elucidated. This article summarizes the research progress of the role of SETD7 on histone and non-histone methylation modification in tumors and the molecular mechanism, in order to provide new therapeutic targets for tumor pathogenesis and diagnosis.
.

摘要

肿瘤的发生和发展是一个复杂的过程,它不仅取决于基因的突变或缺失,还受表观遗传调控的影响。越来越多的证据表明,表观遗传修饰在转录调控、异染色质形成、X染色体失活、DNA损伤反应和肿瘤发展中发挥着重要作用。含SET结构域的赖氨酸甲基转移酶7(SETD7)最初被鉴定为一种重要的赖氨酸甲基转移酶,它可使组蛋白和非组蛋白发生甲基化。这些修饰发挥着重要作用。一旦这种修饰紊乱,可直接导致细胞异常并引发多种疾病。研究表明,SETD7与多种肿瘤的发生和发展有关,但其甲基化位点及其调控机制尚未完全阐明。本文综述了SETD7在肿瘤中对组蛋白和非组蛋白甲基化修饰作用的研究进展及其分子机制,以期为肿瘤发病机制及诊断提供新的治疗靶点。

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2
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本文引用的文献

1
Cyproheptadine, a SET7/9 inhibitor, reduces hyperglycaemia-induced ER stress alleviating inflammation and fibrosis in renal tubular epithelial cells.赛庚啶,一种 SET7/9 抑制剂,可降低高血糖诱导的内质网应激,减轻肾小管上皮细胞的炎症和纤维化。
Arch Physiol Biochem. 2024 Aug;130(4):411-419. doi: 10.1080/13813455.2022.2105365. Epub 2022 Aug 1.
2
The Role of Lysine Methyltransferase SET7/9 in Proliferation and Cell Stress Response.赖氨酸甲基转移酶SET7/9在细胞增殖和应激反应中的作用
Life (Basel). 2022 Mar 2;12(3):362. doi: 10.3390/life12030362.
3
Non-histone Methylation of SET7/9 and its Biological Functions.SET7/9 的非组蛋白甲基化及其生物学功能。
Recent Pat Anticancer Drug Discov. 2022;17(3):231-243. doi: 10.2174/1574892816666211202160041.
4
Set7/9 controls proliferation and genotoxic drug resistance of NSCLC cells.Set7/9 控制非小细胞肺癌细胞的增殖和遗传毒性药物耐药性。
Biochem Biophys Res Commun. 2021 Oct 1;572:41-48. doi: 10.1016/j.bbrc.2021.07.086. Epub 2021 Jul 31.
5
Roles of SET7/9 and LSD1 in the Pathogenesis of Arsenic-induced Hepatocyte Apoptosis.SET7/9和LSD1在砷诱导的肝细胞凋亡发病机制中的作用
J Clin Transl Hepatol. 2021 Jun 28;9(3):364-372. doi: 10.14218/JCTH.2020.00185. Epub 2021 Apr 16.
6
SET7/9 promotes H3K4me3 at lncRNA DRAIC promoter to modulate growth and metastasis of glioma.SET7/9 在长链非编码 RNA DRAIC 启动子上促进 H3K4me3 以调节神经胶质瘤的生长和转移。
Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12241-12250. doi: 10.26355/eurrev_202012_24016.
7
Identification of Differentially Methylated Regions Associated with a Knockout of SUV39H1 in Prostate Cancer Cells.鉴定与前列腺癌细胞 SUV39H1 敲除相关的差异甲基化区域。
Genes (Basel). 2020 Oct 13;11(10):1188. doi: 10.3390/genes11101188.
8
Downregulation of SETD7 promotes migration and invasion of lung cancer cells via JAK2/STAT3 pathway.SETD7 的下调通过 JAK2/STAT3 通路促进肺癌细胞的迁移和侵袭。
Int J Mol Med. 2020 May;45(5):1616-1626. doi: 10.3892/ijmm.2020.4523. Epub 2020 Mar 3.
9
KMT Set7/9 is a new regulator of Sam68 STAR-protein.KMT Set7/9 是 Sam68 STAR 蛋白的一个新调控因子。
Biochem Biophys Res Commun. 2020 May 14;525(4):1018-1024. doi: 10.1016/j.bbrc.2020.03.017. Epub 2020 Mar 13.
10
SET7/9 promotes multiple malignant processes in breast cancer development via RUNX2 activation and is negatively regulated by TRIM21.SET7/9 通过激活 RUNX2 促进乳腺癌发展中的多种恶性过程,并且受到 TRIM21 的负调控。
Cell Death Dis. 2020 Feb 26;11(2):151. doi: 10.1038/s41419-020-2350-2.