Biomolecules 2015, 5(3), 1652-1670; doi:10.3390/biom5031652
Inhibition of Topoisomerase (DNA) I (TOP1): DNA Damage Repair and Anticancer Therapy
School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Mail Drop 64-7520, Pullman, WA 99164, USA
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Academic Editors: Wolf-Dietrich Heyer, Thomas Helleday and Fumio Hanaoka
Received: 22 May 2015 / Accepted: 14 July 2015 / Published: 22 July 2015
(This article belongs to the Special Issue DNA Damage Response)
Abstract
Most chemotherapy regimens contain at least one DNA-damaging agent that preferentially affects the growth of cancer cells. This strategy takes advantage of the differences in cell proliferation between normal and cancer cells. Chemotherapeutic drugs are usually designed to target rapid-dividing cells because sustained proliferation is a common feature of cancer [1,2]. Rapid DNA replication is essential for highly proliferative cells, thus blocking of DNA replication will create numerous mutations and/or chromosome rearrangements—ultimately triggering cell death [3]. Along these lines, DNA topoisomerase inhibitors are of great interest because they help to maintain strand breaks generated by topoisomerases during replication. In this article, we discuss the characteristics of topoisomerase (DNA) I (TOP1) and its inhibitors, as well as the underlying DNA repair pathways and the use of TOP1 inhibitors in cancer therapy. View Full-TextKeywords:
topoisomerase (DNA) I (TOP1); anticancer therapy; DNA replication; topoisomerase inhibitor; DNA double-strand break (DSB); DSB repair; homologous recombination (HR); non-homologous end joining; single-strand break (SSB) repair; one-ended DSB
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Xu, Y.; Her, C. Inhibition of Topoisomerase (DNA) I (TOP1): DNA Damage Repair and Anticancer Therapy. Biomolecules 2015, 5, 1652-1670.
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