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Int J Cancer. 2014 Jan 1;134(1):224-34. doi: 10.1002/ijc.28340. Epub 2013 Jul 24.

IPS-1 plays a dual function to directly induce apoptosis in murine melanoma cells by inactivated Sendai virus.

Author information

1
Comparative Medicine Center, College of Veterinary Medicine, Yangzhou University, Yangzhou, China.

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.

KEYWORDS:

IFN-β promoter stimulator-1; apoptosis; inactivated Sendai virus (HVJ-E); mitogen-activated protein kinase

PMID:
23784981
DOI:
10.1002/ijc.28340
[Indexed for MEDLINE]
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