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.

Abstract

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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