Xing Zhen1, Hu-Nan Sun2, Ren Liu1, Hack Sun Choi3, Dong-Sun Lee4,3,5. 1. Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University, Jeju, Republic of Korea. 2. Department of Disease Model Animal Research Center, College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China. 3. Subtropical/Tropical Organism Gene Bank, Jeju National University, Jeju, Republic of Korea. 4. Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University, Jeju, Republic of Korea dongsunlee@jejunu.ac.kr. 5. Practical Translational Research Center, Jeju National University, Jeju, Republic of Korea.
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. Copyright
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. Copyright
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