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• W1891241630 abstract "Inactivated Sendai virus (HVJ-E) directly kills cancer cells by inducing apoptosis through a mechanism mediated by Janus kinases/signal transducers and activators of transcription (JAK/STAT) signaling pathways. However, whether other signaling pathways are involved remain largely unknown. This study aimed to investigate the mechanism underlying HVJ-E-induced apoptosis in murine B16F10 melanoma cells. We found that HVJ-E induced B16F10 cell apoptosis via the caspase pathway, particularly caspase-9, which mediates the intrinsic apoptotic pathway. Mitogen-activated protein kinase (MAPK) pathway activation also contributed to HVJ-E-induced apoptosis. Whereas caspase pathway involvement depended on both IFN-β promoter stimulator-1 (IPS-1) and type I interferon (IFN), MAPK pathway activation was independent of type I IFN but involved IPS-1. In addition, intratumoral HVJ-E treatment displayed a direct oncolytic effect in an in vivo BALB/c nude mouse melanoma model. Collectively, our data provides new insights into the mechanism underlying HVJ-E-induced apoptosis in tumor cells." @default.
• W1891241630 created "2016-06-24" @default.
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• W1891241630 date "2013-07-24" @default.
• W1891241630 modified "2023-09-25" @default.
• W1891241630 title "IPS-1 plays a dual function to directly induce apoptosis in murine melanoma cells by inactivated Sendai virus" @default.
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• W1891241630 doi "https://doi.org/10.1002/ijc.28340" @default.
• W1891241630 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23784981" @default.
• W1891241630 hasPublicationYear "2013" @default.
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