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Inhibition of the anti-apoptotic BCL-2 and NF-κB pathways restores sensitivity to VSV infection in PC3 cellsPC3 cells were exposed to selective BCL-2 pathway inhibitors (ABT-199 and ABT-737) or a selective NF-κB pathway inhibitor <t>(IKK16)</t> either alone, or in the presence of VSV infection (at an MOI of 50, using either wild-type virus or the attenuated R1 mutant). Cell survival was then quantitated using the PrestoBlue cell viability assay at 24 post-treatment with each drug. Viral infection was initiated 8 h prior to analysis at each timepoint. Data represent the mean ± SEM of 3 biological replicates. **** p < 0.0001, *** p < 0.001, ** p < 0.01 (Student’s t -test).
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Inhibition of the anti-apoptotic BCL-2 and NF-κB pathways restores sensitivity to VSV infection in PC3 cellsPC3 cells were exposed to selective BCL-2 pathway inhibitors (ABT-199 and ABT-737) or a selective NF-κB pathway inhibitor <t>(IKK16)</t> either alone, or in the presence of VSV infection (at an MOI of 50, using either wild-type virus or the attenuated R1 mutant). Cell survival was then quantitated using the PrestoBlue cell viability assay at 24 post-treatment with each drug. Viral infection was initiated 8 h prior to analysis at each timepoint. Data represent the mean ± SEM of 3 biological replicates. **** p < 0.0001, *** p < 0.001, ** p < 0.01 (Student’s t -test).
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Inhibition of the anti-apoptotic BCL-2 and NF-κB pathways restores sensitivity to VSV infection in PC3 cellsPC3 cells were exposed to selective BCL-2 pathway inhibitors (ABT-199 and ABT-737) or a selective NF-κB pathway inhibitor (IKK16) either alone, or in the presence of VSV infection (at an MOI of 50, using either wild-type virus or the attenuated R1 mutant). Cell survival was then quantitated using the PrestoBlue cell viability assay at 24 post-treatment with each drug. Viral infection was initiated 8 h prior to analysis at each timepoint. Data represent the mean ± SEM of 3 biological replicates. **** p < 0.0001, *** p < 0.001, ** p < 0.01 (Student’s t -test).

Journal: bioRxiv

Article Title: Multi-omics Profiling Reveals an NF-κB-Driven Anti-apoptotic Network Underlying Resistance to Oncolytic VSV in Prostate Cancer Cells

doi: 10.64898/2026.06.24.734137

Figure Lengend Snippet: Inhibition of the anti-apoptotic BCL-2 and NF-κB pathways restores sensitivity to VSV infection in PC3 cellsPC3 cells were exposed to selective BCL-2 pathway inhibitors (ABT-199 and ABT-737) or a selective NF-κB pathway inhibitor (IKK16) either alone, or in the presence of VSV infection (at an MOI of 50, using either wild-type virus or the attenuated R1 mutant). Cell survival was then quantitated using the PrestoBlue cell viability assay at 24 post-treatment with each drug. Viral infection was initiated 8 h prior to analysis at each timepoint. Data represent the mean ± SEM of 3 biological replicates. **** p < 0.0001, *** p < 0.001, ** p < 0.01 (Student’s t -test).

Article Snippet: Cells were treated with 5 μM of ABT-199, 5 μM of ABT-737, or 10 μM of IKK16 purchased from Med Chem Express, Monmouth Junction NJ, USA; cat#: HY-15531, HY-50907, HY-13687 (respectively) for 24, 48 and 72 h. 6 h prior to each timepoint, LNCaP cells were infected with an MOI of 10, while at 8 h prior to each timepoint, PC3 cells were infected with an MOI of 50.

Techniques: Inhibition, Infection, Virus, Mutagenesis, Viability Assay