Format

Send to

Choose Destination
Nat Commun. 2015 Apr 20;6:6907. doi: 10.1038/ncomms7907.

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

Author information

1
Department of Polymer┬ĚNano Science and Technology, Polymer Fusion Research Center, Chonbuk National University, Backje-daero 567, Jeonju 561-756, Korea.
2
Department of BIN Convergence Technology, Chonbuk National University, Backje-daero 567, Jeonju 561-756, Korea.
3
1] Department of Polymer┬ĚNano Science and Technology, Polymer Fusion Research Center, Chonbuk National University, Backje-daero 567, Jeonju 561-756, Korea [2] Department of BIN Convergence Technology, Chonbuk National University, Backje-daero 567, Jeonju 561-756, Korea.

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.

PMID:
25892552
DOI:
10.1038/ncomms7907
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center