Int J Biol Sci 2017; 13(7):923-934. doi:10.7150/ijbs.17260 This issue
1. The Science Research Center, Gannan Medical University, Ganzhou 341000, China
2. Institute of Genomic Medicine, Wenzhou Medical University, Wenzhou 325035, China
3. Beijing Institutes of Life Science, Chinese Academy of Sciences, Beijing 100101, China
4. University of Chinese Academy of Sciences, Beijing 100049, China
# Co-first author
Oxidative stress is considered to be a key risk state for a variety of human diseases. In response to oxidative stress, the regulation of transcriptional expression of DNA repair genes would be important to DNA repair and genomic stability. However, the overall pattern of transcriptional expression of DNA repair genes and the underlying molecular response mechanism to oxidative stress remain unclear. Here, by employing colorectal cancer cell lines following exposure to hydrogen peroxide, we generated expression profiles of DNA repair genes via RNA-seq and identified gene subsets that are induced or repressed following oxidative stress exposure. RRBS-seq analyses further indicated that transcriptional regulation of most of the DNA repair genes that were induced or repressed is independent of their DNA methylation status. Our analyses also indicate that hydrogen peroxide induces deacetylase SIRT1 which decreases chromatin affinity and the activity of histone acetyltransferase hMOF toward H4K16ac and results in decreased transcriptional expression of DNA repair genes. Taken together, our findings provide a potential mechanism by which oxidative stress suppresses DNA repair genes which is independent of the DNA methylation status of their promoters.
Keywords: hMOF, H4K16ac, Oxidative Stress