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Chronic Reflux Stress Reshapes the EAC Transcriptional Landscape via APE1

ABSTRACT: Gastroesophageal reflux disease (GERD) is the predominant risk factor for the development of Barrett’s esophagus and esophageal adenocarcinoma (EAC). However, the molecular mechanisms driving responses to chronic reflux conditions in EAC remain poorly defined. This study investigates the genome-wide transcriptional reprogramming and molecular stress responses mediated by apurinic/apyrimidinic endonuclease 1 (APE1) in EAC cells (OE33) surviving chronic, reflux-induced stress. By pairing a 15-day repeated acidified bile salt (rABS) exposure model with subsequent APE1 genetic silencing, this dataset defines the global differential gene expression profiles, altered signaling pathways, and transcriptional networks that depend on APE1 for acquired stress tolerance during sustained reflux insults.

ORGANISM(S): Homo sapiens

PROVIDER: GSE342970 | GEO | 2026/08/11

REPOSITORIES: GEO

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	GSE342970_rABS_RNAseq_Genewiz_2025_12samples_count_matrix.tsv.gz	Tabular

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