期刊
CANCER CELL
卷 28, 期 2, 页码 210-224出版社
CELL PRESS
DOI: 10.1016/j.ccell.2015.06.009
关键词
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资金
- Terry Fox Foundation (TFF) Grant
- Canadian Cancer Society Research Institute (CCSRI)
- Ontario Institute for Cancer Research (OICR)
- Canadian Institute for Health Research (CIHR)
- Ottawa Regional Cancer Foundation
- Ottawa Hospital Foundation
- Mitacs Elevate Industrial Fellowship
- Natural Sciences and Engineering Research Council of Canada (NSERC) scholarship
- NSERC award
- NSERC
- CIHR
- Canadian Breast Cancer Foundation (CBCF)
- fellowship from the Alberta Innovates Health Solutions
- TFF
- CCSRI
- OICR
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. VEG/FNEGFR2 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.
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