Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

RAD51 May Regulate the Expression of Genes Involved in Autophagy Through Interaction with E-box Binding Proteins in Cancer Cell Lines

Version 1 : Received: 20 October 2020 / Approved: 22 October 2020 / Online: 22 October 2020 (09:43:42 CEST)

How to cite: Kang, K.; Choi, Y.; Moon, H.; Seo, M.; Yoon, J.; Beck, B.R.; Kang, K. RAD51 May Regulate the Expression of Genes Involved in Autophagy Through Interaction with E-box Binding Proteins in Cancer Cell Lines. Preprints 2020, 2020100452 (doi: 10.20944/preprints202010.0452.v1). Kang, K.; Choi, Y.; Moon, H.; Seo, M.; Yoon, J.; Beck, B.R.; Kang, K. RAD51 May Regulate the Expression of Genes Involved in Autophagy Through Interaction with E-box Binding Proteins in Cancer Cell Lines. Preprints 2020, 2020100452 (doi: 10.20944/preprints202010.0452.v1).

Abstract

RAD51 is a recombinase that plays a pivotal role in homologous recombination. Although the role of RAD51 in homologous recombination has been extensively studied, it is unclear whether RAD51 can be involved in gene regulation as a co-factor. In this study, we found in silico evidence that RAD51 may contribute to the regulation of genes involved in the autophagy pathway through interaction with E-box proteins such as USF1, USF2, and/or MITF in GM12878, HepG2, K562, and MCF-7 cell lines. The canonical USF binding motif (CACGTG) was significantly identified at RAD51 binding sites in all four cell lines. In addition, genome-wide USF1, USF2, and/or MITF-binding regions significantly coincided with the RAD51-binding sites in the same cell line. Interestingly, the promoters of genes associated with the autophagy pathway were significantly occupied by RAD51 in all four cell lines. Taken together, these results predicted a novel role of RAD51 that had not been addressed previously, and provided evidence that RAD51 could possibly be involved in regulating genes associated with the autophagy pathway, through interaction with E-box binding proteins.

Subject Areas

RAD51; E-box; USF1; USF2; MITF; Cancer cell lines; Gene regulation

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