Abstract
Human cytomegalovirus (HCMV) is a herpesvirus that is prevalent in the human population. HCMV has recently been implicated in different cancer forms where it may provide mechanisms for oncogenic transformation, oncomodulation and tumour cell immune evasion. Moreover, antiviral treatment against HCMV has been shown to inhibit tumour growth in preclinical models. Here we describe the possible involvement of HCMV in cancer and discuss the potential molecular impact expression of HCMV proteins have on tumour cells and the surrounding tumour microenvironment.
Highlights
The interplay between cancer cells and the surrounding microenvironment is essential for the growth and spread of a tumour
This mainly originates from conflicting results regarding the detection of Human cytomegalovirus (HCMV) in tumour samples and since HCMV by itself not has been shown to transform normal cells into cancer cells [47]
The last statement has recently been challenged since the HCMV encoded chemokine receptor homologue US28 renders NIH3T3 cells tumorigenic when injected into nude mice and transgenic mice with targeted expression to intestinal epithelial cells develop intestinal neoplasia [16, 18, 19]
Summary
The interplay between cancer cells and the surrounding microenvironment is essential for the growth and spread of a tumour. Medulloblastoma, neuroblastoma and glioblastoma tumors express high levels of COX-2 and NSAIDs, inhibitors of COX-2 and PGE2 production, have profound effects on the growth of these tumours [64, 94,95,96] These inhibitors efficiently prevent HCMV replication and reduce the growth of US28-expressing tumour cells [17, 18, 70, 73]. Developing drugs that inhibit the functions of HCMV encoded US28 may be of future benefit in cancer treatment since the US28 protein may possess important functions in tumour initiation through the activation of intracellular signalling pathways, angiogenesis and effects on the tumour microenvironment
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