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

Joungyoun Noh, Byeongsu Kwon, Eunji Han, Minhyung Park, Wonseok Yang, Wooram Cho, Wooyoung Yoo, Gilson Khang and Dongwon Lee ()
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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
Dongwon Lee: Polymer Fusion Research Center, Chonbuk National University

Nature Communications, 2015, vol. 6, issue 1, 1-9

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms7907

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