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Research Paper|Volume 13, Issue 8|pp 11170—11187

The critical role of peroxiredoxin-2 in colon cancer stem cells

Linglong Peng1, Yongfu Xiong2, Rong Wang3, Ling Xiang4, He Zhou5, Zhongxue Fu5
  • 1Department of Gastrointestinal Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400014, China
  • 2Department of Hepatobiliary Surgery, The Affiliated Hospital of North Sichuan Medical College, Sichuan 637000, China
  • 3Department of Oncology, The Cancer Center of the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China
  • 4Department of Clinical Nutrition, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400014, China
  • 5Department of Gastrointestinal Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400014, China
* Equal contribution
Received: September 12, 2020Accepted: January 4, 2021Published: March 26, 2021
https://doi.org/10.18632/aging.202784

Copyright: © 2021 Peng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Colon cancer stem cells (CCSCs) play an important role in facilitating colon cancer occurrence, metastasis and drug resistance. The results of our previous studies confirmed that the well-studied antioxidant gene peroxiredoxin-2 (PRDX2) promotes colon cancer progression. However, the underlying function and mechanisms associated with PRDX2 remodeling in the context of CCSCs have remained poorly studied. In our present study, we demonstrated that PRDX2 is highly expressed in CD133/CD44-positive colon cancer tissues and spheroid CD133+CD44+ CCSCs. PRDX2 overexpression was shown to be closely correlated with CD133+CD44+ CCSCs in colon cancer. Furthermore, PRDX2 depletion markedly suppressed CD133+CD44+ CCSC stemness maintenance, tumor initiation, migration and invasion and liver metastasis. Furthermore, the expression of various EMT markers and Wnt/β-catenin signaling proteins was altered after PRDX2 inhibition. In addition, PRDX2 knockdown led to increased ROS production in CD133+CD44+ CCSCs, sensitizing CCSCs to oxidative stress and chemotherapy. These results suggest that PRDX2 could be a possible therapeutic target in CCSCs.