Non-thermal Plasma-activated Medium Induces Apoptosis of Aspc1 Cells Through the ROS-dependent Autophagy Pathway

In Vivo. 2020 Jan-Feb;34(1):143-153. doi: 10.21873/invivo.11755.

Abstract

Background/aim: Numerous studies on various cancer cell lines have reported that direct exposure to non-thermal plasma treatment using plasma-activated medium (PAM) can be applied as a novel technology for cancer therapy. In this study, we investigated the inhibitory effects of PAM on Aspc1 pancreatic cancer cells and the mechanisms responsible for the cell death observed.

Materials and methods: A colony-formation, sphere-formation, wound-healing and transwell assays, immunocytochemistry and western blot analysis were used monitor effects of PAM.

Results: PAM induced a greater cytotoxic effect in pancreatic cancer cells compared to that induced in NIH3T3 cells and 293T cells, and significantly inhibited colony and sphere formation, and cell migration of Aspc1 cells. Furthermore, PAM treatment increased the accumulation of reactive oxygen species (ROS) and reduced the mitochondrial membrane potential in Aspc1 cells. In addition, PAM treatment down-regulated the AKT serine/threonine kinase 1/signal transducer and activator of transcription 3 signaling pathway and induced ROS-dependent cellular autophagy.

Conclusion: Our findings suggest that PAM can induce apoptosis of Aspc1 cells through ROS-dependent autophagy and may be a candidate for use in pancreatic cancer therapeutics.

Keywords: Non-thermal plasma; apoptosis; autophagy; pancreatic cancer; reactive oxygen species.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Autophagy / drug effects*
  • Cell Death / drug effects
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Down-Regulation / drug effects
  • HEK293 Cells
  • Humans
  • Membrane Potential, Mitochondrial / drug effects
  • Mice
  • NIH 3T3 Cells
  • Pancreatic Neoplasms / drug therapy
  • Pancreatic Neoplasms / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Reactive Oxygen Species / metabolism*
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction / drug effects*

Substances

  • Antineoplastic Agents
  • Reactive Oxygen Species
  • STAT3 Transcription Factor
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt