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. Author manuscript; available in PMC: 2020 Jun 1.
Published in final edited form as: Mol Cancer Ther. 2019 Mar 29;18(6):1127–1136. doi: 10.1158/1535-7163.MCT-18-0953

Figure 2. OS2966 inhibits oHSV-mediated anti-viral signaling pathway.

Figure 2.

A-B) Impact of OS2966 on oHSV-induced anti-viral signaling. A) Real time PCR analysis for changes in gene expression of IFNα, IFNβ, and stat1 gene in both patient derived primary GBM (GBM30) and breast cancer cells 24 hours post oHSV treatment. Data presented are fold changes in gene expression ± SD relative to glyceraldehyde-3-phosphate dehydrogenase (GAPDH). B) Real time PCR analysis for changes in a set of the type-I IFN responsive genes involved in the antiviral defense in both patient derived primary GBM (GBM30) and breast cancer cells 24 hours post oHSV treatment. Data presented are relative gene expression between oHSV+OS2966 and oHSV + control IgG. *, p < 0.05. Comparisons made between control IgG versus OS2966 and oHSV versus oHSV+OS2966 treated cells. C) OS2966 inhibits oHSV-induced CCN1 expression and Stat1 activation. Patient derived primary GBM (GBM30) cells were infected with/without 34.5ENVE (MOI=0.01). Two hours post oHSV infection, unbound viruses were removed and 10 ug/ml of control IgG/OS2966 were added and cultured for 24 hours. Cell lysates were probed with antibodies against CCN1, phosphor-Stat1, and total Stat1. β-tubulin was used as a loading control.