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. 2013 Sep 1;2(9):e25620.
doi: 10.4161/onci.25620. Epub 2013 Jul 9.

Mutations in glioblastoma oncosuppressive pathways pave the way for oncomodulatory activity of cytomegalovirus

Todd C Hollon  1 , Richard L Price, Chang-Hyuk Kwon, E Antonio Chiocca
Affiliations

Mutations in glioblastoma oncosuppressive pathways pave the way for oncomodulatory activity of cytomegalovirus

Todd C Hollon et al. Oncoimmunology. .

Abstract

Over the last decade, cytomegalovirus (CMV) has been suggested to promote the development of glioblastoma multiforme (GBM). Recent evidence demonstrates that CMV contributes to the progression of GBM in the context of oncosuppressor gene mutations. This finding provides further insights into the mechanisms whereby CMV exacerbates the malignancy of GBM.

Keywords: brain tumor; glioma; rhabdomyosarcoma; tumor suppressor genes; viral oncology.

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Figures

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Figure 1. Mechanisms of STAT3 activation by CMV. Cytomegalovirus (CMV) can activate signal transducer and activator of transcription 3 (STAT3) in glioblastoma multiforme (GBM) cells by 3 different mechanisms. CMV-infected cells secrete increased levels of interleukin-6 (IL-6), stimulating signal transduction via the IL-6 receptor (IL6R)-STAT3 axis. US28 is a CMV-encoded constitutively active chemokine receptor that is capable of activating STAT3. The CMV virion can activate STAT3 via platelet-derived growth factor receptor α chain (PDGFRα), presumably by means of the viral surface glycoprotein B. The combination of STAT3 activation and oncosuppressor gene loss significantly exacerbates the malignancy of GBM cells.
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