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卡波氏肉瘤相关疱疹病毒的分子生物学与相关致癌作用。

Molecular biology of Kaposi's sarcoma-associated herpesvirus and related oncogenesis.

机构信息

Department of Microbiology, Abramson, Comprehensive Cancer Center, University of Pennsylvania Medical School, Philadelphia, Pennsylvania, USA.

出版信息

Adv Virus Res. 2010;78:87-142. doi: 10.1016/B978-0-12-385032-4.00003-3.

DOI:10.1016/B978-0-12-385032-4.00003-3
PMID:21040832
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3142360/
Abstract

Kaposi's Sarcoma-associated Herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8), is the most recently identified human tumor virus,and is associated with the pathogenesis of Kaposi's sarcoma and two lymphoproliferative disorders known to occur frequently in AIDS patients-primary effusion lymphoma and multicentric Castleman disease. In the 15 years since its discovery, intense studies have demonstrated an etiologic role for KSHV in the development of these malignancies. Here, we review the recent advances linked to understanding KSHV latent and lytic life cycle and the molecular mechanisms of KSHV-mediated oncogenesis in terms of transformation, cell signaling, cell growth and survival, angiogenesis, immune invasion and response to microenvironmental stress, and highlight the potential therapeutic targets for blocking KSHV tumorigenesis.

摘要

卡波济肉瘤相关疱疹病毒(Kaposi's Sarcoma-Associated Herpesvirus,KSHV),也称为人类疱疹病毒 8 型(Human Herpesvirus 8,HHV-8),是最近发现的人类肿瘤病毒,与卡波济肉瘤的发病机制以及两种在艾滋病患者中经常发生的淋巴组织增生性疾病有关,即原发性渗出性淋巴瘤和多中心卡斯特曼病。自发现以来的 15 年中,大量研究表明 KSHV 在这些恶性肿瘤的发生中起病因作用。在这里,我们回顾了与理解 KSHV 潜伏和裂解生命周期以及 KSHV 介导的致癌作用的分子机制相关的最新进展,这些机制涉及转化、细胞信号转导、细胞生长和存活、血管生成、免疫入侵和对微环境压力的反应,并强调了阻断 KSHV 肿瘤发生的潜在治疗靶点。

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Molecular biology of Kaposi's sarcoma-associated herpesvirus and related oncogenesis.卡波氏肉瘤相关疱疹病毒的分子生物学与相关致癌作用。
Adv Virus Res. 2010;78:87-142. doi: 10.1016/B978-0-12-385032-4.00003-3.
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The elevated expression of ORF75, a KSHV lytic gene, in Kaposi sarcoma lesions is driven by a GC-rich DNA cis element in its promoter region.卡波西肉瘤病变中KSHV裂解基因ORF75的高表达是由其启动子区域富含GC的DNA顺式元件驱动的。
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DNA-Binding Activities of KSHV DNA Polymerase Processivity Factor (PF-8) Complexes.

本文引用的文献

1
Kaposi's sarcoma and its associated herpesvirus.卡波氏肉瘤及其相关疱疹病毒。
Nat Rev Cancer. 2010 Oct;10(10):707-19. doi: 10.1038/nrc2888.
2
Kaposi's sarcoma-associated herpesvirus inhibits interleukin-4-mediated STAT6 phosphorylation to regulate apoptosis and maintain latency.卡波氏肉瘤相关疱疹病毒抑制白细胞介素-4 介导的 STAT6 磷酸化,以调节细胞凋亡并维持潜伏状态。
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3
Bub1 and CENP-F can contribute to Kaposi's sarcoma-associated herpesvirus genome persistence by targeting LANA to kinetochores.
卡波西肉瘤相关疱疹病毒DNA聚合酶持续合成因子(PF-8)复合物的DNA结合活性
Viruses. 2025 Jan 29;17(2):190. doi: 10.3390/v17020190.
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Animal models of human herpesvirus infection.人类疱疹病毒感染的动物模型。
Animal Model Exp Med. 2025 Apr;8(4):615-628. doi: 10.1002/ame2.12575. Epub 2025 Feb 7.
5
FoxK1 and FoxK2 cooperate with ORF45 to promote late lytic replication of Kaposi's sarcoma-associated herpesvirus.FoxK1和FoxK2与ORF45协同作用,促进卡波西肉瘤相关疱疹病毒的晚期裂解复制。
J Virol. 2024 Dec 17;98(12):e0077924. doi: 10.1128/jvi.00779-24. Epub 2024 Nov 4.
6
Ubiquitin-Mediated Effects on Oncogenesis during EBV and KSHV Infection.泛素化对 EBV 和 KSHV 感染期间致癌作用的影响。
Viruses. 2024 Sep 26;16(10):1523. doi: 10.3390/v16101523.
7
Human Viral Oncoproteins and Ubiquitin-Proteasome System.人类病毒癌蛋白与泛素-蛋白酶体系统
Glob Med Genet. 2024 Sep 2;11(4):285-296. doi: 10.1055/s-0044-1790210. eCollection 2024 Dec.
8
Kaposi's sarcoma-associated herpesvirus (KSHV) LANA prevents KSHV episomes from degradation.卡波氏肉瘤相关疱疹病毒 (KSHV) 的 LANA 可防止 KSHV 染色体外体降解。
J Virol. 2024 Feb 20;98(2):e0126823. doi: 10.1128/jvi.01268-23. Epub 2024 Jan 19.
9
Disrupting Kaposi's Sarcoma-Associated Herpesvirus (KSHV) Latent Replication with a Small Molecule Inhibitor.用小分子抑制剂破坏卡波西肉瘤相关疱疹病毒(KSHV)潜伏复制。
J Med Chem. 2023 Aug 10;66(15):10782-10790. doi: 10.1021/acs.jmedchem.3c00990. Epub 2023 Jul 28.
10
Onco-Pathogen Mediated Cancer Progression and Associated Signaling Pathways in Cancer Development.肿瘤病原体介导的癌症进展及癌症发展中的相关信号通路
Pathogens. 2023 May 28;12(6):770. doi: 10.3390/pathogens12060770.
Bub1 和 CENP-F 可以通过将 LANA 靶向动粒来促进卡波氏肉瘤相关疱疹病毒基因组的持续存在。
J Virol. 2010 Oct;84(19):9718-32. doi: 10.1128/JVI.00713-10. Epub 2010 Jul 21.
4
Efficacy of bortezomib in a direct xenograft model of primary effusion lymphoma.硼替佐米在原发性渗出性淋巴瘤直接异种移植模型中的疗效。
Proc Natl Acad Sci U S A. 2010 Jul 20;107(29):13069-74. doi: 10.1073/pnas.1002985107. Epub 2010 Jul 6.
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Small RNA profiling reveals antisense transcription throughout the KSHV genome and novel small RNAs.小 RNA 谱分析揭示了整个 KSHV 基因组和新的小 RNA 的反义转录。
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6
Extracellular Hsp90 serves as a co-factor for MAPK activation and latent viral gene expression during de novo infection by KSHV.在由 KSHV 引起的初次感染过程中,细胞外 HSP90 可作为 MAPK 激活和潜伏病毒基因表达的辅助因子。
Virology. 2010 Jul 20;403(1):92-102. doi: 10.1016/j.virol.2010.03.052. Epub 2010 May 6.
7
Accumulation of oxidized proteins in Herpesvirus infected cells.疱疹病毒感染细胞中氧化蛋白质的积累。
Free Radic Biol Med. 2010 Aug 1;49(3):383-91. doi: 10.1016/j.freeradbiomed.2010.04.026. Epub 2010 May 2.
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miR-132 regulates antiviral innate immunity through suppression of the p300 transcriptional co-activator.miR-132 通过抑制 p300 转录共激活因子来调节抗病毒先天免疫。
Nat Cell Biol. 2010 May;12(5):513-9. doi: 10.1038/ncb2054. Epub 2010 Apr 25.
9
Human I-mfa domain proteins specifically interact with KSHV LANA and affect its regulation of Wnt signaling-dependent transcription.人源 I-mfa 结构域蛋白特异性地与 KSHV LANA 相互作用,并影响其对 Wnt 信号依赖性转录的调控。
Biochem Biophys Res Commun. 2010 Jun 4;396(3):608-13. doi: 10.1016/j.bbrc.2010.04.111. Epub 2010 Apr 24.
10
Hypoxia inactivates the VHL tumor suppressor through PIASy-mediated SUMO modification.缺氧通过 PIASy 介导的 SUMO 修饰使 VHL 肿瘤抑制因子失活。
PLoS One. 2010 Mar 16;5(3):e9720. doi: 10.1371/journal.pone.0009720.