NDLI: Using DNA devices to track anticancer drug activity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Boothman, David A. Slinker, Jason D. Kahanda, Dimithree Mcwilliams, Marc A. Chakrabarti, Gaurab
Description	Country affiliation: United States Author Affiliation: Kahanda D ( Department of Physics, The University of Texas at Dallas, 800 W. Campbell Rd., PHY 36, Richardson, TX 75080, United States.); Chakrabarti G ( Departments of Pharmacology, Oncology and Radiation Oncology, Laboratory of Molecular Stress Responses and the Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, ND2.210K 601 Forest Park Drive, Dallas, TX 75390-8807, United States.); Mcwilliams MA ( Department of Physics, The University of Texas at Dallas, 800 W. Campbell Rd., PHY 36, Richardson, TX 75080, United States.); Boothman DA ( Departments of Pharmacology, Oncology and Radiation Oncology, Laboratory of Molecular Stress Responses and the Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, ND2.210K 601 Forest Park Drive, Dallas, TX 75390-8807, United States.); Slinker JD ( Department of Physics, The University of Texas at Dallas, 800 W. Campbell Rd., PHY 36, Richardson, TX 75080, United States. Electronic address: slinker@utdallas.edu.)
Abstract	It is beneficial to develop systems that reproduce complex reactions of biological systems while maintaining control over specific factors involved in such processes. We demonstrated a DNA device for following the repair of DNA damage produced by a redox-cycling anticancer drug, beta-lapachone (ß-lap). These chips supported ß-lap-induced biological redox cycle and tracked subsequent DNA damage repair activity with redox-modified DNA monolayers on gold. We observed drug-specific changes in square wave voltammetry from these chips at therapeutic ß-lap concentrations of high statistical significance over drug-free control. We also demonstrated a high correlation of this change with the specific ß-lap-induced redox cycle using rational controls. The concentration dependence of ß-lap revealed significant signal changes at levels of high clinical significance as well as sensitivity to sub-lethal levels of ß-lap. Catalase, an enzyme decomposing peroxide, was found to suppress DNA damage at a NQO1/catalase ratio found in healthy cells, but was clearly overcome at a higher NQO1/catalase ratio consistent with cancer cells. We found that it was necessary to reproduce key features of the cellular environment to observe this activity. Thus, this chip-based platform enabled tracking of ß-lap-induced DNA damage repair when biological criteria were met, providing a unique synthetic platform for uncovering activity normally confined to inside cells.
ISSN	09565663
Volume Number	80
e-ISSN	18734235
Journal	Biosensors and Bioelectronics
Language	English
Publisher	Elsevier
Publisher Date	2016-06-15
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Antineoplastic Agents Pharmacology Biosensing Techniques Dna Repair Catalase Chemistry Cell Line, Tumor Dna Damage Drug Effects Gold Humans Nad(p)h Dehydrogenase (quinone) Naphthoquinones Journal Article Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Biotechnology
Content Type	Text
Resource Type	Article
Subject	Nanoscience and Nanotechnology Medicine Biophysics Biomedical Engineering Biotechnology Electrochemistry

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