Volume 29 Issue 12
Dec.  2016
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GAO Hui, LI Ling Yu, ZHANG Man, ZHANG Quan. Inactivated Sendai Virus Induces Apoptosis Mediated by Reactive Oxygen Species in Murine Melanoma Cells[J]. Biomedical and Environmental Sciences, 2016, 29(12): 877-884. doi: 10.3967/bes2016.117
Citation: GAO Hui, LI Ling Yu, ZHANG Man, ZHANG Quan. Inactivated Sendai Virus Induces Apoptosis Mediated by Reactive Oxygen Species in Murine Melanoma Cells[J]. Biomedical and Environmental Sciences, 2016, 29(12): 877-884. doi: 10.3967/bes2016.117

Inactivated Sendai Virus Induces Apoptosis Mediated by Reactive Oxygen Species in Murine Melanoma Cells

doi: 10.3967/bes2016.117
Funds:  the National Natural Science foundation of China(31302042)%the Natural Science Foundation of Jiangsu Province(BK20130445)%the Priority Academic Program Development of Jiangsu Higher Education Institutions, and the Young and Middle-aged Academic Leaders Plan of Yangzhou University
  • Objective This paper aims to investigate the apoptotic effect of inactivated Sendai virus (hemagglutinating virus of Japan-enveloped, HVJ-E) on murine melanoma cells (B16F10) and the possible mechanisms involved in the putative apoptotic reactions. Methods B16F10 cells were treated with HVJ-E at various multiplicities of infection (MOI), and the reactive oxygen species (ROS), cell viability, and apoptosis were measured. Next, the roles of ROS in the regulation of Bcl-2/Bax and the activation of mitogen-activated protein kinase (MAPK) pathways in HVJ-E-treated B16F10 cells were analyzed. To further evaluate the cytotoxic effect of HVJ-E-generated ROS on B16F10 cells, HVJ-E was intratumorally injected, both with and without N-acetyl-L-cysteine (NAC), into melanoma tumors on BALB/c mice. Tumor volume was then monitored for 3 weeks, and the tumor proteins were separated for immunoblot assay. Results Treatment of B16F10 cells with HVJ-E resulted in a dose-dependent inhibition of cell-viability and an induction of apoptosis. The latter effect was associated with the generation of ROS. Inhibition of ROS generation by NAC resulted in a significant reduction of HVJ-E-induced Erk1/2, JNK, and p38 MAPK activation. Additionally, ROS inhibition caused a decrease in the Bcl-2/Bax ratio as well as promoting activation of apoptosis both in vitro and in vivo. Conclusion These results suggest that HVJ-E possesses potential anticancer activity in B16F10 cells through ROS-mediated mitochondrial dysfunction involving the MAPK pathway.
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    沈阳化工大学材料科学与工程学院 沈阳 110142

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Inactivated Sendai Virus Induces Apoptosis Mediated by Reactive Oxygen Species in Murine Melanoma Cells

doi: 10.3967/bes2016.117
Funds:  the National Natural Science foundation of China(31302042)%the Natural Science Foundation of Jiangsu Province(BK20130445)%the Priority Academic Program Development of Jiangsu Higher Education Institutions, and the Young and Middle-aged Academic Leaders Plan of Yangzhou University

Abstract: Objective This paper aims to investigate the apoptotic effect of inactivated Sendai virus (hemagglutinating virus of Japan-enveloped, HVJ-E) on murine melanoma cells (B16F10) and the possible mechanisms involved in the putative apoptotic reactions. Methods B16F10 cells were treated with HVJ-E at various multiplicities of infection (MOI), and the reactive oxygen species (ROS), cell viability, and apoptosis were measured. Next, the roles of ROS in the regulation of Bcl-2/Bax and the activation of mitogen-activated protein kinase (MAPK) pathways in HVJ-E-treated B16F10 cells were analyzed. To further evaluate the cytotoxic effect of HVJ-E-generated ROS on B16F10 cells, HVJ-E was intratumorally injected, both with and without N-acetyl-L-cysteine (NAC), into melanoma tumors on BALB/c mice. Tumor volume was then monitored for 3 weeks, and the tumor proteins were separated for immunoblot assay. Results Treatment of B16F10 cells with HVJ-E resulted in a dose-dependent inhibition of cell-viability and an induction of apoptosis. The latter effect was associated with the generation of ROS. Inhibition of ROS generation by NAC resulted in a significant reduction of HVJ-E-induced Erk1/2, JNK, and p38 MAPK activation. Additionally, ROS inhibition caused a decrease in the Bcl-2/Bax ratio as well as promoting activation of apoptosis both in vitro and in vivo. Conclusion These results suggest that HVJ-E possesses potential anticancer activity in B16F10 cells through ROS-mediated mitochondrial dysfunction involving the MAPK pathway.

GAO Hui, LI Ling Yu, ZHANG Man, ZHANG Quan. Inactivated Sendai Virus Induces Apoptosis Mediated by Reactive Oxygen Species in Murine Melanoma Cells[J]. Biomedical and Environmental Sciences, 2016, 29(12): 877-884. doi: 10.3967/bes2016.117
Citation: GAO Hui, LI Ling Yu, ZHANG Man, ZHANG Quan. Inactivated Sendai Virus Induces Apoptosis Mediated by Reactive Oxygen Species in Murine Melanoma Cells[J]. Biomedical and Environmental Sciences, 2016, 29(12): 877-884. doi: 10.3967/bes2016.117

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