Open AccessRAD51 Inhibitor Reverses Etoposide-Induced Genomic Toxicity and Instability in Esophageal Adenocarcinoma Cells
Author(s) -
Chengcheng Liao,
Jiangning Zhao,
Subodh Kumar,
Chitraleema Chakraborty,
Srikanth Talluri,
Nikhil C. Munshi,
Masood A. Shammas
Publication year - 2020
Publication title -
pubmed central
Language(s) - English
Resource type - Journals
eISSN - 2692-8280
DOI - 10.46439/toxicology.2.006
Subject(s) - rad51 , genome instability , etoposide , dna damage , homologous recombination , cancer research , dna repair , biology , genomic dna , viability assay , cytotoxicity , microbiology and biotechnology , chemistry , apoptosis , dna , genetics , chemotherapy , in vitro
In normal cells, homologous recombination (HR) is strictly regulated and precise and plays an important role in preserving genomic integrity by accurately repairing DNA damage. RAD51 is the recombinase which mediates homologous base pairing and strand exchange during DNA repair by HR. We have previously reported that HR is spontaneously elevated (or dysregulated) in esophageal adenocarcinoma (EAC) and contributes to ongoing genomic changes and instability. The purpose of this study was to evaluate the impact of RAD51 inhibitor on genomic toxicity caused by etoposide, a chemotherapeutic agent.