Long-Term Alteration of Reactive Oxygen Species Led to Multidrug Resistance in MCF-7 CellsReport as inadecuate




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Oxidative Medicine and Cellular Longevity - Volume 2016 2016, Article ID 7053451, 15 pages -

Research Article

Key Laboratory of Natural Medicine and Immune Engineering, Henan University, Kaifeng, China

School of Pharmacy, Henan University, Kaifeng, China

Received 18 August 2016; Revised 25 October 2016; Accepted 6 November 2016

Academic Editor: Jacek Zielonka

Copyright © 2016 Juan Cen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Reactive oxygen species ROS play an important role in multidrug resistance MDR. This study aimed to investigate the effects of long-term ROS alteration on MDR in MCF-7 cells and to explore its underlying mechanism. Our study showed both long-term treatments of H2O2 and glutathione GSH led to MDR with suppressed iROS levels in MCF-7 cells. Moreover, the MDR cells induced by 0.1 μM H2O2 treatment for 20 weeks MCF-7-ROS cells had a higher viability and proliferative ability than the control MCF-7 cells. MCF-7-ROS cells also showed higher activity or content of intracellular antioxidants like glutathione peroxidase GPx, GSH, superoxide dismutase SOD, and catalase CAT. Importantly, MCF-7-ROS cells were characterized by overexpression of MDR-related protein 1 MRP1 and P-glycoprotein P-gp, as well as their regulators NF-E2-related factor 2 Nrf2, hypoxia-inducible factor 1 HIF-1α, and the activation of PI3K-Akt pathway in upstream. Moreover, several typical MDR mediators, including glutathione S-transferase-π GST-π and c-Myc and Protein Kinase Cα PKCα, were also found to be upregulated in MCF-7-ROS cells. Collectively, our results suggest that ROS may be critical in the generation of MDR, which may provide new insights into understanding of mechanisms of MDR.





Author: Juan Cen, Li Zhang, Fangfang Liu, Feng Zhang, and Bian-Sheng Ji

Source: https://www.hindawi.com/



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