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Figure S1. VPA stimulates H-1PV-mediated oncolysis in cervical and pancreatic derived cancer cell lines.

Figure S2. H-1PV/VPA co-treatment is not harmful to normal primary human cells.

Figure S3. The HDAC inhibitor NaB synergizes with H-1PV in killing HeLa cells by inducing ROS accumulation and DNA damage.

Figure S4. NaB increases NS1-mediated cytotoxicity.

Figure S5. NaB treatment increases H-1PV expression.

Figure S6. VPA increases H-1PV production in cervical carcinoma derived cell lines.

Figure S7. VPA enhances H-1PV oncosuppressive capacity in the HeLa xenograft rat model.

Figure S8. Virus biodistribution in H-1PV/VPA-co-treated animals after tumour eradication.

Figure S9. Analysis of HeLa all-derived tumours for the presence of the human papillomavirus genome.

Figure S10. Complete remission of established AsPC-1 tumours upon combined treatment with H-1PV and VPA.

Figure S11. Morphological analysis of AsPC-1 cell tumour xenografts.

Figure S12. H-1PV/VPA co-treatment leads to complete eradication of established primary tumour material xenografts.

Table S1. Summary of statistical analysis results obtained for cancer cell lines co-treated with H-1PV and VPA.

Table S2. Summary of statistical analysis results obtained for HeLa and AsPC-1 animal experiments.

emmm201302796-SourceData-Fig1.pdfPDF document252KSource Data for Figure 1
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