Abstract
Reprogramming of energy metabolism is a key for cancer development. Kaposi’s sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated by three pathways of central carbon metabolism, including aerobic glycolysis, glutaminolysis, and fatty acid synthesis. Increasing evidence has shown that KSHV infection can alter central carbon metabolic pathways to produce biomass for viral replication, as well as the survival and proliferation of infected cells. In this review, we summarize recent studies exploring how KSHV manipulates host cell metabolism to promote viral pathogenesis, which provides the potential therapeutic targets and strategies for KSHV-associated cancers.
Highlights
Reprogramming of energy metabolism is a hallmark of cancers
We summarize most recent studies regarding to how Kaposi’s sarcoma-associated herpesvirus (KSHV) alters host cellular metabolism for viral production and oncogenesis, three major pathways of cellular metabolism including central carbon metabolism, aerobic glycolysis, glutaminolysis and fatty acid synthesis are addressed and discussed below (Figure 1)
The profile analysis of high-throughput RNA sequencing has revealed that the expression levels of many enzymes in the glutamine pathway are upregulated by KSHV infection, which supports the notion that KSHV mediates host cellular glutaminolysis for promoting proliferation of KSHVtransformed cells (Sanchez et al, 2015; Zhu et al, 2017)
Summary
Reprogramming of energy metabolism is a key for cancer development. Kaposi’s sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated by three pathways of central carbon metabolism, including aerobic glycolysis, glutaminolysis, and fatty acid synthesis. Increasing evidence has shown that KSHV infection can alter central carbon metabolic pathways to produce biomass for viral replication, as well as the survival and proliferation of infected cells. We summarize recent studies exploring how KSHV manipulates host cell metabolism to promote viral pathogenesis, which provides the potential therapeutic targets and strategies for KSHV-associated cancers
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