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. 2020;1(1):10-15.
doi: 10.46439/cancerbiology.1.003.

Role of H3K9 demethylases in DNA double-strand break repair

Hee-Young Jeon  1   2 , Arif Hussain  2   3 , Jianfei Qi  1   2
Affiliations

Role of H3K9 demethylases in DNA double-strand break repair

Hee-Young Jeon et al. J Cancer Biol. 2020.

Abstract

H3K9 demethylases can remove the repressive H3K9 methylation marks on histones to alter chromatin structure, gene transcription and epigenetic state of cells. By counteracting the function of H3K9 methyltransferases, H3K9 demethylases have been shown to play an important role in numerous biological processes, including diseases such as cancer. Recent evidence points to a key role for some H3K9 demethylases in the repair of DNA double-strand breaks (DSBs) via homologous recombination (HR) and/or non-homologous end joining (NHEJ) pathways. Mechanistically, H3K9 demethylases can upregulate the expression of DNA repair factors. They can also be recruited to the DNA damage sites and regulate the recruitment or function of DNA repair factors. Here, we will discuss the role and mechanisms of H3K9 demethylases in the regulation of DSB repair.

Keywords: DNA damage repair; H3K9; cancer; demethylation; double-strand breaks; epigenetic; histone demethylase.

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Conflict of interest statement

Conflicts of Interest The authors declare no conflicts of interest.

Figures

Figure 1.
Figure 1.
JMJD1A activity in prostate cancer cells increases the level of c-Myc and also enhances the c-Myc chromatin recruitment by demethylating H3K9me2 marks on the gene promoters of indicated DNA repair factors for HR or NHEJ. JMJD1A may also regulate the activity of another unidentified transcription factor to upregulate the expression of RNF8. The elevated expression of these DNA repair factors leads to the enhanced DSB repair by both HR and NHEJ pathways. Thus, JMJD1A activity contributes to the resistance of prostate cancer cells to IR, topoisomerase inhibitors or PARP inhibitors.
See this image and copyright information in PMC

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