Upregulation of peroxiredoxin III in doxorubicin-induced cytotoxicity and the FoxO3a-dependent expression in H9c2 cardiac cells

  • Authors:
    • Mi‑Hua Liu
    • Yuan Zhang
    • Jun He
    • Tian‑Ping Tan
    • Shao‑Jian Wu
    • Hong‑Yun Fu
    • Yu‑Dan Chen
    • Jun Liu
    • Qun‑Fang Le
    • Heng‑Jing Hu
    • Cong Yuan
    • Xiao‑Long Lin
  • View Affiliations

  • Published online on: August 20, 2015     https://doi.org/10.3892/etm.2015.2693
  • Pages: 1515-1520
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Abstract

Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it produces reactive oxygen species (ROS) that induce severe cytotoxicity, limiting its clinical application. The aim of the present study was to investigate the role of peroxiredoxin III (Prx III) in DOX‑induced H9c2 cell injuries. Following DOX treatment, the expression of phosphorylated‑FoxO3a (p‑FoxO3a) was decreased and Prx III expression was increased in H9c2 cells. In order to detect whether oxidative stress was involved in the induction of Prx III expression by FoxO3a, exogenous H2O2 was used to induce oxidative stress in the H9c2 cells. Apoptosis of H9c2 cardiomyocytes was assessed using methyl thiazolyl tetrazolium assay and Hoechst staining. The levels of Prx III and p‑FoxO3a were evaluated using western blot analysis. As expected, H2O2 was found to mimic the effect of DOX, decreasing the expression of p‑FoxO3a and increasing the expression of Prx III. In addition, the study evaluated whether the transcription factor FoxO3a was essential for the expression of Prx III. Pretreatment of H9c2 cells with N‑acetyl‑L‑cysteine (NAC), a scavenger of ROS, prior to exposure to DOX dramatically increased the phosphorylation of FoxO3a and led to a marked reduction in Prx III expression in the H9c2 cells. In conclusion, the results of the current study suggest that FoxO3a mediates the expression of Prx III in DOX-induced injuries.
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October-2015
Volume 10 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Liu MH, Zhang Y, He J, Tan TP, Wu SJ, Fu HY, Chen YD, Liu J, Le QF, Hu HJ, Hu HJ, et al: Upregulation of peroxiredoxin III in doxorubicin-induced cytotoxicity and the FoxO3a-dependent expression in H9c2 cardiac cells. Exp Ther Med 10: 1515-1520, 2015.
APA
Liu, M., Zhang, Y., He, J., Tan, T., Wu, S., Fu, H. ... Lin, X. (2015). Upregulation of peroxiredoxin III in doxorubicin-induced cytotoxicity and the FoxO3a-dependent expression in H9c2 cardiac cells. Experimental and Therapeutic Medicine, 10, 1515-1520. https://doi.org/10.3892/etm.2015.2693
MLA
Liu, M., Zhang, Y., He, J., Tan, T., Wu, S., Fu, H., Chen, Y., Liu, J., Le, Q., Hu, H., Yuan, C., Lin, X."Upregulation of peroxiredoxin III in doxorubicin-induced cytotoxicity and the FoxO3a-dependent expression in H9c2 cardiac cells". Experimental and Therapeutic Medicine 10.4 (2015): 1515-1520.
Chicago
Liu, M., Zhang, Y., He, J., Tan, T., Wu, S., Fu, H., Chen, Y., Liu, J., Le, Q., Hu, H., Yuan, C., Lin, X."Upregulation of peroxiredoxin III in doxorubicin-induced cytotoxicity and the FoxO3a-dependent expression in H9c2 cardiac cells". Experimental and Therapeutic Medicine 10, no. 4 (2015): 1515-1520. https://doi.org/10.3892/etm.2015.2693