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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 1. OS2966 treatment inhibits focal adhesion kinase (FAK)-Akt signal pathway and enhances oHSV replication and oHSV-mediated tumor cell killing.

Figure 1.

A) patient derived primary GBM (GBM12) and MDA468 breast cancer 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 phospho-FAK (S397), total FAK, phosphor Akt (S473), total Akt, and cleaved PARP which is downstream of integrin β1-FAK signaling. GAPDH was used as a loading control. B) Patient derived primary GBM cells (GBM30) were plated on Laminin (LM)-, or Fibronectin (FN)-coated plates and infected with 34.5ENVE (MOI=0.002). Two hours later, unbound viruses were removed and cultured for 72 hours. Fluorescence microscope images of GFP-positive infected GBM30 cells. C-D) The indicated cells were plated on LM-, or FN-coated plates and infected with 34.5ENVE. Two hours later, unbound viruses were removed and cells were treated with 10 μg/ml of control IgG or OS2966. Viral titers were measured by standard plaque forming unit assay (C) and cell viability was measured by MTT assay (D) 72 hours post oHSV infection. *: p < 0.05 compared to oHSV + control IgG. *: p < 0.05 compared to oHSV + control IgG.