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Published on: April 23, 2014
Inactivated Sendai Virus Induces ROS-dependent Apoptosis and Autophagy in Human Prostate Cancer Cells
Miao Qian1, Hai Ming Tan1, Ning Yu1
1Institute of Comparative Medicine, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, Jiangsu, China.
Objective:
The current study aims to investigate the effect of Hemagglutinating virus of Japan envelope (HVJ-E) on induction of apoptosis and autophagy in human prostate cancer PC3 cells, and the underlying mechanisms.
Methods:
PC3 cells were treated with HVJ-E at various multiplicity of infection (MOI), and the generated reactive oxygen species (ROS), cell viability, apoptosis, and autophagy were detected, respectively. Next, the role of ROS played in the regulation of HVJ-E-induced apoptosis and autuphagy in PC3 cells were analysed. In the end, the relationship between HVJ-E-induced apoptosis and autuophagy was investigated by using rapamycin and chloroquine.
Results:
Flow cytometry assay revealed that HVJ-E treatment induced dose-dependent apoptosis and that the JNK and p38 MAPK signaling pathways were involved in HVJ-E-induced apoptosis in PC3 cells. In addition, HVJ-E was able to induce autophagy in PC3 cells via the class III PI3K/beclin-1 pathway. The data also implyed that HVJ-E-triggered autophagy and apoptosis were ROS dependent. When ROS was blocked with N-acetylcysteine (NAC), HVJ-E-induced LC3-II conversion and apoptosis were reversed. Interestingly, HVJ-E-induced apoptosis was significantly increased by an inducer of autophagy, rapamycin pretreatment, both in vitro and in vivo.
Conclusion:
HVJ-E exerts anticancer effects via autophagic cell death in prostate cancer cells.
Insights
Hemagglutinating virus of Japan envelope (HVJ-E) induces apoptosis and autophagy in prostate cancer cells. This virus triggers cell death through reactive oxygen species (ROS) and enhances apoptosis when autophagy is induced.
Area of Science:
- Oncology
- Virology
- Cell Biology
Background:
- Prostate cancer remains a significant health concern with ongoing research for novel therapeutic strategies.
- Understanding the mechanisms of cell death induction is crucial for developing effective cancer treatments.
Purpose of the Study:
- To investigate the effects of Hemagglutinating virus of Japan envelope (HVJ-E) on apoptosis and autophagy in human prostate cancer PC3 cells.
- To elucidate the underlying molecular mechanisms, including the role of reactive oxygen species (ROS) and specific signaling pathways.
Main Methods:
- PC3 cells were treated with varying multiplicities of infection (MOI) of HVJ-E.
- Assays were performed to detect reactive oxygen species (ROS), cell viability, apoptosis, and autophagy.
- Inhibitors and inducers of autophagy (rapamycin, chloroquine) and ROS (N-acetylcysteine) were used to analyze pathway involvement.
Main Results:
- HVJ-E induced dose-dependent apoptosis in PC3 cells, involving JNK and p38 MAPK pathways.
- HVJ-E triggered autophagy via the class III PI3K/beclin-1 pathway.
- Both HVJ-E-induced autophagy and apoptosis were dependent on ROS; blocking ROS reversed these effects.
- Autophagy induction with rapamycin enhanced HVJ-E-induced apoptosis.
Conclusions:
- HVJ-E demonstrates anticancer effects in prostate cancer cells by inducing autophagic cell death.
- The findings suggest HVJ-E as a potential therapeutic agent for prostate cancer, acting through ROS-mediated apoptosis and autophagy.
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