Fig. 2: Schematic diagram of potential mechanisms for KSHV promoting HERV transactivation. | Oncogenesis

Fig. 2: Schematic diagram of potential mechanisms for KSHV promoting HERV transactivation.

From: Transactivation of human endogenous retroviruses by tumor viruses and their functions in virus-associated malignancies

Fig. 2

During KSHV de novo infection, LANA induces env transcripts through enhancing ERK activity, and vFLIP induces env transcripts through activating NF-κB activity. Np9 expression mediated by KSHV can promote virus-induced anchorage-independent growth (AIG) and invasion through the CD147-ADAMTS1/ADAMTS9-VEGF/VEGFR1 axis. LANA: a latency-associated nuclear antigen; vFLIP: viral FADD-like interleukin-1-β-converting enzyme (FLICE)/caspase-8-inhibitory protein; ERK: extracellular-signal-regulated kinase; ADAMTS1: a disintegrin and metalloproteinase with thrombospondin motifs 1; ADAMTS9: a disintegrin and metalloproteinase with thrombospondin motifs 9; VEGF: vascular endothelial growth factor; VEGFR1: vascular endothelial growth factor receptor 1

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