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Arecoline-regulated ataxia telangiectasia mutated expression level in oral cancer progression
- Source :
- Head & Neck. 41:2525-2537
- Publication Year :
- 2019
- Publisher :
- Wiley, 2019.
-
Abstract
- BACKGROUND Ataxia telangiectasia mutated (ATM) regulates DNA repair and cell cycle. The present study analyzed arecoline-induced ATM expression during oral cancer progression. METHODS In vitro studies were performed using oral squamous cell carcinoma (OSCC) cell lines treated with arecoline to analyze cell response and ATM regulation. in vivo studies were performed using immunohistochemistry to detect ATM expression in normal, oral potentially malignant disorder (OPMD), and OSCC tissues. RESULTS Low-dose arecoline induced cell proliferation, ATM promoter activity, and DNA repair. High-dose arecoline induced cell cycle arrest, apoptosis, and DNA damage. ATM was overexpressed in OPMD tissues but was downregulated in OSCC tissues. ATM expression level was associated with the risk of developing dysplasia, buccal-OSCC, and with OSCC survival rate. CONCLUSION High ATM expression helps DNA repair mechanisms to maintain the cells in the OPMD stage, but low ATM expression causes DNA damage accumulation to increase cell malignancy.
- Subjects :
- 0301 basic medicine
Cell cycle checkpoint
DNA Repair
DNA damage
DNA repair
Arecoline
Cell
Apoptosis
Ataxia Telangiectasia Mutated Proteins
03 medical and health sciences
0302 clinical medicine
Cell Line, Tumor
medicine
Humans
Promoter Regions, Genetic
Cell Proliferation
Dose-Response Relationship, Drug
Cell growth
business.industry
Cancer
Cell Cycle Checkpoints
Cell cycle
medicine.disease
Immunohistochemistry
stomatognathic diseases
030104 developmental biology
medicine.anatomical_structure
Otorhinolaryngology
030220 oncology & carcinogenesis
Carcinoma, Squamous Cell
Disease Progression
Cancer research
Mouth Neoplasms
business
DNA Damage
medicine.drug
Subjects
Details
- ISSN :
- 10433074
- Volume :
- 41
- Database :
- OpenAIRE
- Journal :
- Head & Neck
- Accession number :
- edsair.doi.dedup.....d6ce2b7da62b3cc2716c173ca1fa3d28