Combination treatment with arsenic trioxide and sulindac induces apoptosis of NCI-H157 human lung carcinoma cells via ROS generation with mitochondrial dysfunction

Tuberculosis and Respiratory Diseases

Volumn 59, Issue 1, 2005, Pages 30-38

  Kim, Hak Ryul ^a,b   Yang, Sei Hoon ^a   Jeong, Eun Taik ^a  

^a Wonkwang University   (South Korea)

^b Wonkwang University Hospital   (South Korea)

Author keywords

Apoptosis; Arsenic trioxide; Sulindac

Indexed keywords

3 (4,5 DIMETHYL 2 THIAZOLYL) 2,5 DIPHENYLTETRAZOLIUM BROMIDE; ACETYLCYSTEINE; AMRUBICIN; ANTHRACYCLINE ANTIBIOTIC AGENT; ANTIOXIDANT; ARSENIC TRIOXIDE; CASPASE; CISPLATIN; CYTOCHROME C; DOCETAXEL; ETOPOSIDE; GLUTATHIONE; HORSERADISH PEROXIDASE; HYDROGEN PEROXIDE; IRINOTECAN; NIMESULIDE; NONSTEROID ANTIINFLAMMATORY AGENT; PACLITAXEL; PROTEIN BCL 2; REACTIVE OXYGEN METABOLITE; SCOPOLETIN; SULINDAC; VINCA ALKALOID;

APOPTOSIS; ARTICLE; CANCER CELL CULTURE; CANCER CHEMOTHERAPY; CANCER RADIOTHERAPY; CELL PROTECTION; CELL STRAIN NCI H157; CELL VIABILITY; CONTROLLED STUDY; DOSE RESPONSE; DRUG POTENTIATION; ENZYME ACTIVATION; ENZYME RELEASE; FLUOROMETRY; HUMAN; HUMAN CELL; LUNG CARCINOMA; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; OXIDATIVE STRESS; PROTEIN EXPRESSION; PROTEIN FAMILY; SIGNAL TRANSDUCTION; WESTERN BLOTTING;

EID: 26044453635     PISSN: 17383536     EISSN: None     Source Type: Journal    
DOI: 10.4046/trd.2005.59.1.30     Document Type: Article

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