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Amplification of oxidative stress by a dual stimuli-responsive hybrid drug enhances cancer cell death

Author

Listed:
  • Joungyoun Noh

    (Polymer Fusion Research Center, Chonbuk National University)

  • Byeongsu Kwon

    (Chonbuk National University)

  • Eunji Han

    (Chonbuk National University)

  • Minhyung Park

    (Chonbuk National University)

  • Wonseok Yang

    (Chonbuk National University)

  • Wooram Cho

    (Chonbuk National University)

  • Wooyoung Yoo

    (Chonbuk National University)

  • Gilson Khang

    (Polymer Fusion Research Center, Chonbuk National University
    Chonbuk National University)

  • Dongwon Lee

    (Polymer Fusion Research Center, Chonbuk National University
    Chonbuk National University)

Abstract

Cancer cells, compared with normal cells, are under oxidative stress associated with the increased generation of reactive oxygen species (ROS) including H2O2 and are also susceptible to further ROS insults. Cancer cells adapt to oxidative stress by upregulating antioxidant systems such as glutathione to counteract the damaging effects of ROS. Therefore, the elevation of oxidative stress preferentially in cancer cells by depleting glutathione or generating ROS is a logical therapeutic strategy for the development of anticancer drugs. Here we report a dual stimuli-responsive hybrid anticancer drug QCA, which can be activated by H2O2 and acidic pH to release glutathione-scavenging quinone methide and ROS-generating cinnamaldehyde, respectively, in cancer cells. Quinone methide and cinnamaldehyde act in a synergistic manner to amplify oxidative stress, leading to preferential killing of cancer cells in vitro and in vivo. We therefore anticipate that QCA has promising potential as an anticancer therapeutic agent.

Suggested Citation

  • Joungyoun Noh & Byeongsu Kwon & Eunji Han & Minhyung Park & Wonseok Yang & Wooram Cho & Wooyoung Yoo & Gilson Khang & Dongwon Lee, 2015. "Amplification of oxidative stress by a dual stimuli-responsive hybrid drug enhances cancer cell death," Nature Communications, Nature, vol. 6(1), pages 1-9, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7907
    DOI: 10.1038/ncomms7907
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