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Research ArticleExperimental Studies

Peroxiredoxin V Silencing Elevates Susceptibility to Doxorubicin-induced Cell Apoptosis via ROS-dependent Mitochondrial Dysfunction in AGS Gastric Cancer Cells

YONG-ZHE JIN, YI-XI GONG, YUE LIU, DAN-PING XIE, CHEN-XI REN, SEUNG-JAE LEE, HU-NAN SUN, TAEHO KWON and DONG-YUAN XU
Anticancer Research April 2021, 41 (4) 1831-1840; DOI: https://doi.org/10.21873/anticanres.14949
YONG-ZHE JIN
1School of Nursing, Yanbian University, Yanji, P.R. China;
2College of Medicine, Yanbian University, Yanji, P.R. China;
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YI-XI GONG
3College of Life Science & Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China;
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YUE LIU
3College of Life Science & Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China;
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DAN-PING XIE
3College of Life Science & Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China;
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CHEN-XI REN
3College of Life Science & Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China;
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SEUNG-JAE LEE
4Immunoregulatory Materials Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk, Republic of Korea;
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HU-NAN SUN
3College of Life Science & Technology, Heilongjiang Bayi Agricultural University, Daqing, P.R. China;
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  • For correspondence: kwon@kribb.re.kr sunhunan76@163.com dyxu@ybu.edu.cn
TAEHO KWON
5Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeonbuk, Republic of Korea
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  • For correspondence: kwon@kribb.re.kr sunhunan76@163.com dyxu@ybu.edu.cn
DONG-YUAN XU
2College of Medicine, Yanbian University, Yanji, P.R. China;
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  • For correspondence: kwon@kribb.re.kr sunhunan76@163.com dyxu@ybu.edu.cn
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Abstract

Background/Aim: Peroxiredoxin V (Prx V) plays crucial roles in cellular apoptosis and proliferation in various cancer cells by regulating the cellular reactive oxygen species (ROS) levels. Materials and Methods: Here, we examined the possible regulatory effects of Prx V on doxorubicin (DOX)-induced cellular apoptosis and its mechanisms in the human gastric adenocarcinoma cell line (AGS cells). Results: Our findings suggest that Prx V knockdown may significantly increase the DOX-induced apoptosis by aggravating intracellular ROS accumulation. We also found that DOX-induced mitochondrial ROS levels and membrane permeability were significantly higher in short hairpin Prx V cells than in mock cells, and these phenomena were dramatically reversed by ROS scavenger treatment. Prx V knockdown also significantly upregulated the cleaved caspase 9, 3, and B-cell lymphoma 2 (Bcl2)-associated agonist of cell death/Bcl2 protein expression levels, suggesting that Prx V knockdown activates mitochondria-dependent apoptotic signaling pathways. Conclusion: Taken together, this study suggests that Prx V may be a strong molecular target for gastric cancer (GC) chemotherapy, and further elucidates the role of Prx V in oxidative stress-induced cell apoptosis.

Key Words:
  • Peroxiredoxin V
  • reactive oxygen species
  • apoptosis
  • mitochondria
  • gastric cancer
  • Received January 14, 2021.
  • Revision received February 15, 2021.
  • Accepted February 16, 2021.
  • Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.
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Anticancer Research: 41 (4)
Anticancer Research
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April 2021
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Peroxiredoxin V Silencing Elevates Susceptibility to Doxorubicin-induced Cell Apoptosis via ROS-dependent Mitochondrial Dysfunction in AGS Gastric Cancer Cells
YONG-ZHE JIN, YI-XI GONG, YUE LIU, DAN-PING XIE, CHEN-XI REN, SEUNG-JAE LEE, HU-NAN SUN, TAEHO KWON, DONG-YUAN XU
Anticancer Research Apr 2021, 41 (4) 1831-1840; DOI: 10.21873/anticanres.14949

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Peroxiredoxin V Silencing Elevates Susceptibility to Doxorubicin-induced Cell Apoptosis via ROS-dependent Mitochondrial Dysfunction in AGS Gastric Cancer Cells
YONG-ZHE JIN, YI-XI GONG, YUE LIU, DAN-PING XIE, CHEN-XI REN, SEUNG-JAE LEE, HU-NAN SUN, TAEHO KWON, DONG-YUAN XU
Anticancer Research Apr 2021, 41 (4) 1831-1840; DOI: 10.21873/anticanres.14949
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Keywords

  • Peroxiredoxin V
  • reactive oxygen species
  • apoptosis
  • mitochondria
  • gastric cancer
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