Non-thermal Plasma-activated Medium Induces Apoptosis of Aspc1 Cells Through the ROS-dependent Autophagy Pathway
Xing Zhen1, Hu-Nan Sun2, Ren Liu1
1Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University, Jeju, Republic of Korea.
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.
Insights
Plasma-activated medium (PAM) effectively inhibits pancreatic cancer cell growth and migration. PAM induces cancer cell death through reactive oxygen species (ROS)-dependent autophagy, showing potential as a novel pancreatic cancer therapy.
Area of Science:
- Biomedical Engineering
- Cancer Research
- Cell Biology
Background:
- Non-thermal plasma treatment, utilizing plasma-activated medium (PAM), is an emerging technology for cancer therapy.
- Previous studies demonstrated PAM's efficacy across various cancer cell lines.
Purpose of the Study:
- To investigate the inhibitory effects of PAM on Aspc1 pancreatic cancer cells.
- To elucidate the mechanisms underlying PAM-induced cell death in pancreatic cancer.
Main Methods:
- Colony-formation, sphere-formation, wound-healing, and transwell assays were employed.
- Immunocytochemistry and Western blot analyses were conducted to assess cellular changes.
- Reactive oxygen species (ROS) levels and mitochondrial membrane potential were measured.
Main Results:
- PAM exhibited a significant cytotoxic effect on Aspc1 cells compared to normal cells.
- PAM inhibited colony and sphere formation, as well as cell migration in Aspc1 cells.
- PAM induced ROS accumulation, reduced mitochondrial membrane potential, and triggered ROS-dependent autophagy, down-regulating the AKT/STAT3 pathway.
Conclusions:
- PAM demonstrates potent anti-cancer effects on Aspc1 pancreatic cancer cells.
- The mechanism involves ROS-dependent autophagy, leading to apoptosis.
- PAM shows promise as a potential therapeutic agent for pancreatic cancer.
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