RAD51 Inhibitor Reverses Etoposide-Induced Genomic Toxicity and Instability in Esophageal Adenocarcinoma Cells | Zendy

Chengcheng Liao | Zendy; Jiangning Zhao | Zendy; Subodh Kumar | Zendy; Chandraditya Chakraborty | Zendy; Srikanth Talluri | Zendy; Nikhil C. Munshi | Zendy; Masood A. Shammas | Zendy

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RAD51 Inhibitor Reverses Etoposide-Induced Genomic Toxicity and Instability in Esophageal Adenocarcinoma Cells

Author(s) -

Chengcheng Liao,

Jiangning Zhao,

Subodh Kumar,

Chandraditya Chakraborty,

Srikanth Talluri,

Nikhil C. Munshi,

Masood A. Shammas

Publication year - 2020

Publication title -

archives of clinical toxicology

Language(s) - English

Resource type - Journals

ISSN - 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.

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