Instigation of Notch signaling in the pathogenesis of Kaposi's sarcoma-associated herpesvirus and other human tumor viruses

被引:1
作者
Cheng, Fang [1 ,2 ,3 ]
Pekkonen, Pirita [1 ,2 ]
Ojala, Paivi M. [1 ,2 ,4 ]
机构
[1] Univ Helsinki, Inst Biotechnol, Helsinki 00014, Finland
[2] Univ Helsinki, Res Programs Unit, FIN-00014 Helsinki, Finland
[3] Abo Akad Univ, Turku Ctr Biotechnol, BioCity, Turku 20521, Finland
[4] Fdn Finnish Canc Inst, Helsinki, Finland
关键词
EndMT; human tumor virus; KSHV; Notch pathway; RBP-J kappa; viral reactivation; RBP-J-KAPPA; INTRACELLULAR-ACTIVATED NOTCH1; TO-MESENCHYMAL TRANSITION; MAJOR DOWNSTREAM EFFECTOR; PRIMARY EFFUSION LYMPHOMA; CERVICAL-CANCER CELLS; LYTIC SWITCH PROTEIN; NUCLEAR ANTIGEN; GENE-EXPRESSION; ENDOTHELIAL-CELLS;
D O I
10.2217/FMB.12.95
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The Notch pathway is a highly conserved signaling circuit with a critical role in cell-fate determination and tumor initiation. Notch is reported to regulate various key events in tumor progression, such as angiogenesis, maintenance of cancer stem cells, resistance to therapeutic agents and metastasis. This review describes the intimate interplay of human tumor viruses with the Notch signaling pathway. Special attention is paid to Kaposi's sarcoma-associated herpesvirus, the etiological agent of Kaposi's sarcoma and rare lymphoproliferative disorders. The past decade of active research has led to significant advances in understanding how Kaposi's sarcoma-associated herpesvirus exploits the Notch pathway to regulate its replication phase and to modulate the host cellular microenvironment to make it more favorable for viral persistence and spreading.
引用
收藏
页码:1191 / 1205
页数:15
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