Abstract:
:Oncolytic viruses designed to attack malignant cells can in addition infect and destroy tumor vascular endothelial cells. We show here that this expanded tropism of oncolytic vaccinia virus to the endothelial compartment is a consequence of VEGF-mediated suppression of the intrinsic antiviral response. VEGF/VEGFR2 signaling through Erk1/2 and Stat3 leads to upregulation, nuclear localization, and activation of the transcription repressor PRD1-BF1/Blimp1. PRD1-BF1 does not contribute to the mitogenic effects of VEGF, but directly represses genes involved in type I interferon (IFN)-mediated antiviral signaling. In vivo suppression of VEGF signaling diminishes PRD1-BF1/Blimp1 expression in tumor vasculature and inhibits intravenously administered oncolytic vaccinia delivery to and consequent spread within the tumor.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Arulanandam R,Batenchuk C,Angarita FA,Ottolino-Perry K,Cousineau S,Mottashed A,Burgess E,Falls TJ,De Silva N,Tsang J,Howe GA,Bourgeois-Daigneault MC,Conrad DP,Daneshmand M,Breitbach CJ,Kirn DH,Raptis L,Sad S,Atkins Hdoi
10.1016/j.ccell.2015.06.009subject
Has Abstractpub_date
2015-08-10 00:00:00pages
210-24issue
2eissn
1535-6108issn
1878-3686pii
S1535-6108(15)00219-6journal_volume
28pub_type
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