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1
E box-dependent activation of telomerase by human papillomavirus type 16 E6 does not require induction of c-myc.人乳头瘤病毒16型E6对端粒酶的E盒依赖性激活并不需要诱导c-myc。
J Virol. 2001 Aug;75(15):7198-201. doi: 10.1128/JVI.75.15.7198-7201.2001.
2
Telomerase activation by human papillomavirus type 16 E6 protein: induction of human telomerase reverse transcriptase expression through Myc and GC-rich Sp1 binding sites.人乳头瘤病毒16型E6蛋白激活端粒酶：通过Myc和富含GC的Sp1结合位点诱导人端粒酶逆转录酶表达。
J Virol. 2001 Jun;75(12):5559-66. doi: 10.1128/JVI.75.12.5559-5566.2001.
3
Transcriptional activation of the telomerase hTERT gene by human papillomavirus type 16 E6 oncoprotein.人乳头瘤病毒16型E6癌蛋白对端粒酶hTERT基因的转录激活作用
J Virol. 2001 May;75(9):4467-72. doi: 10.1128/JVI.75.9.4467-4472.2001.
4
The E6AP ubiquitin ligase is required for transactivation of the hTERT promoter by the human papillomavirus E6 oncoprotein.人乳头瘤病毒E6癌蛋白对hTERT启动子进行反式激活需要E6AP泛素连接酶。
J Biol Chem. 2005 Mar 18;280(11):10807-16. doi: 10.1074/jbc.M410343200. Epub 2005 Jan 17.
5
Cell-restricted immortalization by human papillomavirus correlates with telomerase activation and engagement of the hTERT promoter by Myc.人乳头瘤病毒介导的细胞限制性永生化与端粒酶激活以及Myc对hTERT启动子的结合相关。
J Virol. 2008 Dec;82(23):11568-76. doi: 10.1128/JVI.01318-08. Epub 2008 Sep 25.
6
Human papillomavirus E6 and Myc proteins associate in vivo and bind to and cooperatively activate the telomerase reverse transcriptase promoter.人乳头瘤病毒E6蛋白和Myc蛋白在体内相互作用，结合并协同激活端粒酶逆转录酶启动子。
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8211-6. doi: 10.1073/pnas.1435900100. Epub 2003 Jun 23.
7
HPV16-E6 associated hTERT promoter acetylation is E6AP dependent, increased in later passage cells and enhanced by loss of p300.人乳头瘤病毒16型E6（HPV16-E6）相关的端粒酶逆转录酶（hTERT）启动子乙酰化依赖于E6相关蛋白（E6AP），在传代后期细胞中增加，并因p300缺失而增强。
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Regulation of telomerase by human papillomaviruses.人乳头瘤病毒对端粒酶的调控
Cold Spring Harb Symp Quant Biol. 2005;70:209-15. doi: 10.1101/sqb.2005.70.041.
10
Identification of a novel telomerase repressor that interacts with the human papillomavirus type-16 E6/E6-AP complex.一种与16型人乳头瘤病毒E6/E6-AP复合物相互作用的新型端粒酶抑制因子的鉴定。
Genes Dev. 2004 Sep 15;18(18):2269-82. doi: 10.1101/gad.1214704.

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HPV and HCMV in Cervical Cancer: A Review of Their Co-Occurrence in Premalignant and Malignant Lesions.人乳头瘤病毒（HPV）和巨细胞病毒（HCMV）与宫颈癌：癌前病变和恶性病变中共同发生的综述。
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HPV-YAP1 oncogenic alliance drives malignant transformation of fallopian tube epithelial cells.HPV-YAP1 致癌联盟驱动输卵管上皮细胞的恶性转化。
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AIB1 is a novel target of the high-risk HPV E6 protein and a biomarker of cervical cancer progression.AIB1 是高危型 HPV E6 蛋白的一个新靶标，也是宫颈癌进展的一个生物标志物。
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7
Human Papillomaviruses Target the DNA Damage Repair and Innate Immune Response Pathways to Allow for Persistent Infection.人乳头瘤病毒靶向 DNA 损伤修复和固有免疫反应途径，以允许持续感染。
Viruses. 2021 Jul 17;13(7):1390. doi: 10.3390/v13071390.
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Exploring the Roles of HERC2 and the NEDD4L HECT E3 Ubiquitin Ligase Subfamily in p53 Signaling and the DNA Damage Response.探索HERC2和NEDD4L HECT E3泛素连接酶亚家族在p53信号通路及DNA损伤反应中的作用
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9
Human papillomavirus E6 and E7: What remains?人乳头瘤病毒 E6 和 E7：还有什么？
Tumour Virus Res. 2021 Jun;11:200213. doi: 10.1016/j.tvr.2021.200213. Epub 2021 Feb 8.
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HIV-1 Protease Inhibitors Slow HPV16-Driven Cell Proliferation through Targeted Depletion of Viral E6 and E7 Oncoproteins.HIV-1蛋白酶抑制剂通过靶向清除病毒E6和E7癌蛋白减缓HPV16驱动的细胞增殖。
Cancers (Basel). 2021 Feb 24;13(5):949. doi: 10.3390/cancers13050949.

本文引用的文献

1
Transcriptional activation of the telomerase hTERT gene by human papillomavirus type 16 E6 oncoprotein.人乳头瘤病毒16型E6癌蛋白对端粒酶hTERT基因的转录激活作用
J Virol. 2001 May;75(9):4467-72. doi: 10.1128/JVI.75.9.4467-4472.2001.
2
Human papillomavirus type 16 E6-induced degradation of E6TP1 correlates with its ability to immortalize human mammary epithelial cells.人乳头瘤病毒16型E6诱导的E6TP1降解与其使人类乳腺上皮细胞永生化的能力相关。
J Virol. 2001 May;75(9):4459-66. doi: 10.1128/JVI.75.9.4459-4466.2001.
3
Human breast cancer cells generated by oncogenic transformation of primary mammary epithelial cells.由原代乳腺上皮细胞致癌转化产生的人乳腺癌细胞。
Genes Dev. 2001 Jan 1;15(1):50-65. doi: 10.1101/gad.828901.
4
Molecular interactions between telomerase and the tumor suppressor protein p53 in vitro.端粒酶与肿瘤抑制蛋白p53在体外的分子相互作用。
Oncogene. 1999 Nov 18;18(48):6785-94. doi: 10.1038/sj.onc.1203061.
5
Adenovirus-mediated p53 gene transduction inhibits telomerase activity independent of its effects on cell cycle arrest and apoptosis in human pancreatic cancer cells.腺病毒介导的p53基因转导抑制人胰腺癌细胞中的端粒酶活性，且该作用独立于其对细胞周期阻滞和细胞凋亡的影响。
Clin Cancer Res. 1999 Aug;5(8):2140-7.
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Creation of human tumour cells with defined genetic elements.利用特定遗传元件创建人类肿瘤细胞。
Nature. 1999 Jul 29;400(6743):464-8. doi: 10.1038/22780.
7
Multiple functions of human papillomavirus type 16 E6 contribute to the immortalization of mammary epithelial cells.人乳头瘤病毒16型E6的多种功能有助于乳腺上皮细胞的永生化。
J Virol. 1999 Sep;73(9):7297-307. doi: 10.1128/JVI.73.9.7297-7307.1999.
8
Genomic organization and promoter characterization of the gene encoding the human telomerase reverse transcriptase (hTERT).人类端粒酶逆转录酶（hTERT）编码基因的基因组结构与启动子特征分析
Gene. 1999 May 17;232(1):97-106. doi: 10.1016/s0378-1119(99)00108-0.
9
Viral oncogenes accelerate conversion to immortality of cultured conditionally immortal human mammary epithelial cells.病毒癌基因可加速培养的条件性永生化人乳腺上皮细胞向永生化状态的转变。
Oncogene. 1999 Apr 1;18(13):2169-80. doi: 10.1038/sj.onc.1202523.
10
Cloning and characterization of the promoter region of human telomerase reverse transcriptase gene.人端粒酶逆转录酶基因启动子区域的克隆与鉴定
Cancer Res. 1999 Feb 15;59(4):826-30.

人乳头瘤病毒16型E6对端粒酶的E盒依赖性激活并不需要诱导c-myc。

E box-dependent activation of telomerase by human papillomavirus type 16 E6 does not require induction of c-myc.

作者信息

Gewin L, Galloway D A

机构信息

Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.

出版信息

J Virol. 2001 Aug;75(15):7198-201. doi: 10.1128/JVI.75.15.7198-7201.2001.

DOI:10.1128/JVI.75.15.7198-7201.2001
PMID:11435602
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC114450/
Abstract

Human papillomavirus type 16 (HPV-16) E6 activates telomerase specifically in epithelial cells. The oncogene c-myc has also been shown to activate telomerase in several cell types. Here we show that while both HPV-16 E6 and c-myc require intact E boxes to transactivate the hTERT promoter, E6 does not induce hTERT transcription simply by inducing expression of c-myc. Moreover, hTERT transactivation by HPV-16 E6 correlates with its ability to bind the cellular E6-associated protein (E6AP), suggesting that E6 and E6AP may target a regulator of hTERT expression.

摘要

人乳头瘤病毒16型（HPV - 16）E6蛋白特异性地激活上皮细胞中的端粒酶。致癌基因c - myc也已证实在多种细胞类型中可激活端粒酶。在此我们表明，虽然HPV - 16 E6蛋白和c - myc都需要完整的E盒来反式激活hTERT启动子，但E6蛋白并非简单地通过诱导c - myc的表达来诱导hTERT转录。此外，HPV - 16 E6蛋白对hTERT的反式激活与其结合细胞E6相关蛋白（E6AP）的能力相关，这表明E6蛋白和E6AP可能靶向hTERT表达的一种调节因子。