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

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Article: e25620 | Received 01 Jul 2013, Accepted 02 Jul 2013, Published online: 09 Jul 2013

Figures & data

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.Citation8 US28 is a CMV-encoded constitutively active chemokine receptor that is capable of activating STAT3.Citation9 The CMV virion can activate STAT3 via platelet-derived growth factor receptor α chain (PDGFRα), presumably by means of the viral surface glycoprotein B.Citation10 The combination of STAT3 activation and oncosuppressor gene loss significantly exacerbates the malignancy of GBM cells.

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.Citation8 US28 is a CMV-encoded constitutively active chemokine receptor that is capable of activating STAT3.Citation9 The CMV virion can activate STAT3 via platelet-derived growth factor receptor α chain (PDGFRα), presumably by means of the viral surface glycoprotein B.Citation10 The combination of STAT3 activation and oncosuppressor gene loss significantly exacerbates the malignancy of GBM cells.