DMCA
Werner Syndrome Protein, WRN, Protects Cells from DNA Damage Induced by the Benzene Metabolite Hydroquinone (2008)
| Citations: | 2 - 0 self |
BibTeX
@MISC{Ren08wernersyndrome,
author = {Xuefeng Ren and Sophia Lim and Martyn T. Smith and Luoping Zhang},
title = {Werner Syndrome Protein, WRN, Protects Cells from DNA Damage Induced by the Benzene Metabolite Hydroquinone},
year = {2008}
}
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Abstract
Werner syndrome (WS) is a rare autosomal progeroid disorder caused by a mutation in the gene encoding the WRN (Werner syndrome protein), a member of the RecQ family of helicases with a role in maintaining genomic stability. Genetic association studies have previously suggested a link between WRN and susceptibility to benzene-induced hematotoxicity. To further explore the role of WRN in benzene-induced hematotoxicity, we used short hairpin RNA to silence endogenous levels of WRN in the human HL60 acute promyelocytic cell line and subsequently exposed the cells to hydroquinone (HQ). Suppression of WRN led to an accelerated cell growth rate, increased susceptibility to hydroquinone-induced cytotoxicity and genotoxicity as measured by the single-cell gel electrophoresis assay, and an enhanced DNA damage response. More specifically, loss of WRN resulted in higher levels of early apoptosis, marked by increases in relative levels of cleaved
Keyphrases
dna damage induced werner syndrome protein benzene metabolite hydroquinone protects cell benzene-induced hematotoxicity rare autosomal progeroid disorder endogenous level werner syndrome early apoptosis hydroquinone-induced cytotoxicity relative level genomic stability cell growth rate genetic association study short hairpin rna single-cell gel electrophoresis assay recq family enhanced dna damage response
