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CYLD and HCC: when being too sensitive to your dirty neighbors results in self-destruction.CYLD 和 HCC:当对肮脏的邻居过于敏感导致自我毁灭时。
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The expression of tumor suppressor gene Cyld is upregulated by histone deacetylace inhibitors in human hepatocellular carcinoma cell lines.在人肝癌细胞系中,组蛋白去乙酰化酶抑制剂可上调肿瘤抑制基因Cyld的表达。
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Down-regulation of CYLD as a trigger for NF-κB activation and a mechanism of apoptotic resistance in hepatocellular carcinoma cells.CYLD 的下调作为 NF-κB 激活的触发因素和肝癌细胞凋亡抵抗的机制。
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Anti-oncogenic effects of SOX2 silencing on hepatocellular carcinoma achieved by upregulating miR-222-5p-dependent CYLD via the long noncoding RNA CCAT1.通过长链非编码 RNA CCAT1 上调 miR-222-5p 依赖性 CYLD,实现 SOX2 沉默对肝癌的抑癌作用。
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Cylindromatosis gene CYLD regulates hepatocyte growth factor expression in hepatic stellate cells through interaction with histone deacetylase 7.Cylindromatosis 基因 CYLD 通过与组蛋白去乙酰化酶 7 的相互作用调节肝星状细胞中肝细胞生长因子的表达。
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Adenoviral vector expressing CYLD augments antitumor activity of TRAIL by suppression of NF-kappaB survival signaling in hepatocellular carcinoma.表达CYLD的腺病毒载体通过抑制肝细胞癌中的NF-κB生存信号增强TRAIL的抗肿瘤活性。
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CYLD controls c-MYC expression through the JNK-dependent signaling pathway in hepatocellular carcinoma.CYLD 通过 JNK 依赖的信号通路控制肝癌细胞中的 c-MYC 表达。
Carcinogenesis. 2014 Feb;35(2):461-8. doi: 10.1093/carcin/bgt335. Epub 2013 Oct 8.
8
MiR-501-5p regulates CYLD expression and promotes cell proliferation in human hepatocellular carcinoma.微小RNA-501-5p调节CYLD表达并促进人肝细胞癌的细胞增殖。
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Regulation of early wave of germ cell apoptosis and spermatogenesis by deubiquitinating enzyme CYLD.去泛素化酶CYLD对生殖细胞早期凋亡和精子发生的调控
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[Research progress of deubiquitinating enzyme CYLD to regulate liver-related diseases].去泛素化酶CYLD调控肝脏相关疾病的研究进展
Zhonghua Gan Zang Bing Za Zhi. 2019 Jun 20;27(6):477-480. doi: 10.3760/cma.j.issn.1007-3418.2019.06.019.

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Emerging roles of deubiquitinating enzymes in actin cytoskeleton and tumor metastasis.去泛素化酶在肌动蛋白细胞骨架和肿瘤转移中的新兴作用。
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miR‑197‑3p‑induced downregulation of lysine 63 deubiquitinase promotes cell proliferation and inhibits cell apoptosis in lung adenocarcinoma cell lines.miR-197-3p 诱导的赖氨酸 63 去泛素化酶下调促进肺腺癌细胞系的细胞增殖并抑制细胞凋亡。
Mol Med Rep. 2018 Mar;17(3):3921-3927. doi: 10.3892/mmr.2017.8333. Epub 2017 Dec 20.
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Genetic alterations in TRAF3 and CYLD that regulate nuclear factor κB and interferon signaling define head and neck cancer subsets harboring human papillomavirus.TRAF3 和 CYLD 中的遗传改变调节核因子 κB 和干扰素信号,定义了携带人乳头瘤病毒的头颈部癌症亚群。
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Downregulation of miR-362-5p inhibits proliferation, migration and invasion of human breast cancer MCF7 cells.miR-362-5p的下调抑制人乳腺癌MCF7细胞的增殖、迁移和侵袭。
Oncol Lett. 2016 Feb;11(2):1155-1160. doi: 10.3892/ol.2015.3993. Epub 2015 Dec 3.

本文引用的文献

1
Inactivation of the deubiquitinase CYLD in hepatocytes causes apoptosis, inflammation, fibrosis, and cancer.肝细胞中去泛素化酶 CYLD 的失活会导致细胞凋亡、炎症、纤维化和癌症。
Cancer Cell. 2012 Jun 12;21(6):738-50. doi: 10.1016/j.ccr.2012.04.026.
2
Promotion of hepatocellular carcinoma by the intestinal microbiota and TLR4.肠道微生物群和 TLR4 促进肝细胞癌的发生。
Cancer Cell. 2012 Apr 17;21(4):504-16. doi: 10.1016/j.ccr.2012.02.007.
3
TAK1 suppresses a NEMO-dependent but NF-kappaB-independent pathway to liver cancer.TAK1 抑制了一种依赖于 NEMO 但不依赖于 NF-κB 的肝癌发生途径。
Cancer Cell. 2010 May 18;17(5):481-96. doi: 10.1016/j.ccr.2010.03.021.
4
Disruption of TAK1 in hepatocytes causes hepatic injury, inflammation, fibrosis, and carcinogenesis.TAK1 在肝细胞中的缺失会导致肝损伤、炎症、纤维化和癌变。
Proc Natl Acad Sci U S A. 2010 Jan 12;107(2):844-9. doi: 10.1073/pnas.0909781107. Epub 2009 Dec 18.
5
Deletion of NEMO/IKKgamma in liver parenchymal cells causes steatohepatitis and hepatocellular carcinoma.肝实质细胞中NEMO/IKKγ的缺失会导致脂肪性肝炎和肝细胞癌。
Cancer Cell. 2007 Feb;11(2):119-32. doi: 10.1016/j.ccr.2006.12.016.
6
Loss of hepatic NF-kappa B activity enhances chemical hepatocarcinogenesis through sustained c-Jun N-terminal kinase 1 activation.肝脏核因子-κB活性丧失通过持续激活c-Jun氨基末端激酶1增强化学性肝癌发生。
Proc Natl Acad Sci U S A. 2006 Jul 11;103(28):10544-51. doi: 10.1073/pnas.0603499103. Epub 2006 Jun 28.
7
IKKbeta couples hepatocyte death to cytokine-driven compensatory proliferation that promotes chemical hepatocarcinogenesis.IKKβ 将肝细胞死亡与细胞因子驱动的代偿性增殖联系起来,这种增殖促进化学性肝癌发生。
Cell. 2005 Jul 1;121(7):977-90. doi: 10.1016/j.cell.2005.04.014.
8
NF-kappaB functions as a tumour promoter in inflammation-associated cancer.核因子-κB在炎症相关癌症中作为肿瘤促进因子发挥作用。
Nature. 2004 Sep 23;431(7007):461-6. doi: 10.1038/nature02924. Epub 2004 Aug 25.

CYLD 和 HCC:当对肮脏的邻居过于敏感导致自我毁灭时。

CYLD and HCC: when being too sensitive to your dirty neighbors results in self-destruction.

机构信息

Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.

出版信息

Cancer Cell. 2012 Jun 12;21(6):711-2. doi: 10.1016/j.ccr.2012.05.034.

DOI:10.1016/j.ccr.2012.05.034
PMID:22698394
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4718070/
Abstract

Hepatocellular carcinoma is the outcome of ongoing cycles of cell death and regeneration in chronic liver disease. In this issue of Cancer Cell, Nikolaou et al. show that the deubiquitinating enzyme CYLD is critical for controlling the balance between hepatocyte loss, regeneration, and malignant progression.

摘要

肝细胞癌是慢性肝病中细胞死亡和再生不断循环的结果。在本期《癌细胞》杂志中,Nikolaou 等人表明去泛素化酶 CYLD 对于控制肝细胞丢失、再生和恶性进展之间的平衡至关重要。