SOX17 overexpression sensitizes chemoradiation response in esophageal cancer by transcriptional down-regulation of DNA repair and damage response genes.
I-Ying KuoYu-Lin HuangChien-Yu LinChien-Hsun LinWei-Lun ChangWu-Wei LaiYing-Jan WangPublished in: Journal of biomedical science (2019)
Our study reveals a novel mechanism by which SOX17 transcriptionally inactivates DNA repair and damage response-related genes to sensitize ESCC cell or xenograft to CCRT treatment. In addition, we establish a proof-of-concept CCRT prediction biomarker using SOX17 immunohistochemical staining in pre-treatment endoscopic biopsies to identify ESCC patients who are at high risk of CCRT failure and need intensive care.
Keyphrases
- dna repair
- transcription factor
- dna damage
- stem cells
- end stage renal disease
- dna damage response
- oxidative stress
- chronic kidney disease
- newly diagnosed
- ejection fraction
- ultrasound guided
- squamous cell carcinoma
- rectal cancer
- single cell
- prognostic factors
- cell therapy
- peritoneal dialysis
- radiation therapy
- replacement therapy
- combination therapy
- induced apoptosis
- patient reported
- locally advanced
- heat shock protein
- smoking cessation