Abstract
Angiogenesis is the biological process by which new blood vessels are formed from pre-existing vessels. It is considered one of the classic hallmarks of cancer, as pathological angiogenesis provides oxygen and essential nutrients to growing tumors. Two of the seven known human oncoviruses, Epstein–Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV), belong to the Gammaherpesvirinae subfamily. Both viruses are associated with several malignancies including lymphomas, nasopharyngeal carcinomas, and Kaposi’s sarcoma. The viral genomes code for a plethora of viral factors, including proteins and non-coding RNAs, some of which have been shown to deregulate angiogenic pathways and promote tumor growth. In this review, we discuss the ability of both viruses to modulate the pro-angiogenic process.
Highlights
The worldwide prevalence of human cancers caused by infectious agents has been estimated to be approximately 15–20% (Plummer et al, 2016)
In addition to promoting vascular endothelial growth factor (VEGF), BZLF1 induces the expression of tissue inhibitor of metalloproteinase (TIMP) 1, which is involved in the modulation of matrix metalloproteinase enzymes (MMPs) and plays a role in viral tumorigenesis by acting as an antiapoptotic protein (Guedez et al, 2001; Lin et al, 2015)
Angiogenesis is one of the hallmarks of cancer, and the ability of a tumor to hijack this process for its benefit facilitates growth and enhances its ability to metastasize (Hanahan and Weinberg, 2011)
Summary
The worldwide prevalence of human cancers caused by infectious agents has been estimated to be approximately 15–20% (Plummer et al, 2016). Following the induction of expression, these pro-angiogenic factors are secreted from the tumor cells and intercellularly bind and activate their respective receptors in endothelial cells (Figure 2). EBV, through LMP1 and other viral genes, induces several growth factor receptors that contribute to the promotion of angiogenesis.
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