Targeting APE1-Redox Function Reverses SOX9-mediated Chemoresistance in Esophageal Adenocarcinoma - PubMed
4 hours ago
- #Chemoresistance
- #APE1-Redox
- #SOX9
- Targeting APE1's redox function reverses SOX9-mediated chemoresistance in esophageal adenocarcinoma (EAC).
- SOX9 molecular signature is significantly enriched in EAC patients and linked to poor relapse-free survival.
- APE1's redox activity stabilizes SOX9 protein, driving chemoresistance under reflux-mimicking conditions and oxaliplatin treatment.
- Pharmacological inhibition of APE1's redox function (e.g., APX2009) downregulates SOX9 and enhances oxaliplatin response in patient-derived xenograft tumors.
- Co-overexpression of APE1 and SOX9, along with Aldehyde Dehydrogenase 1 Family Member A1, is observed in EAC lesions.
- APE1 redox inhibition presents a therapeutic strategy to target the 'undruggable' SOX9 transcription network in EAC.