Involvement of endoplasmic reticulum stress and activation of MAP kinases in β-lapachone-induced human prostate cancer cell apoptosis

Histology and Histopathology

Volumn 23, Issue 11, 2008, Pages 1299-1308

  Lien, Yi Chen ^a   Kung, Hsiu Ni ^b   Lu, Kuo Shyan ^b   Jeng, Chung Jiuan ^a   Chau, Yat Pang ^a  

^a NATIONAL YANG MING UNIVERSITY   (Taiwan)

^b NATIONAL TAIWAN UNIVERSITY   (Taiwan)

Author keywords

Lapachone; Endoplasmic Reticulum (ER) stress; MAPK phosphorylation

Indexed keywords

BETA LAPACHONE; CALCIUM; CALPAIN; CASPASE 12; CASPASE 7; DICOUMAROL; GLUCOSE REGULATED PROTEIN 78; GROWTH ARREST AND DNA DAMAGE INDUCIBLE PROTEIN 153; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE P38; STRESS ACTIVATED PROTEIN KINASE; ANTINEOPLASTIC AGENT; BETA-LAPACHONE; CASPASE; CHELATING AGENT; ENZYME INHIBITOR; NAPHTHOQUINONE; NQO1 PROTEIN, HUMAN; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE (PHOSPHATE) DEHYDROGENASE (QUINONE); UNCLASSIFIED DRUG;

ANTINEOPLASTIC ACTIVITY; APOPTOSIS; ARTICLE; CALCIUM CELL LEVEL; CANCER CELL; CONCENTRATION RESPONSE; CONTROLLED STUDY; ENDOPLASMIC RETICULUM STRESS; ENZYME ACTIVATION; ENZYME INHIBITION; ENZYME PHOSPHORYLATION; HUMAN; HUMAN CELL; PROSTATE CANCER; PROTEIN DEGRADATION; PROTEIN EXPRESSION; PROTEIN INDUCTION; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; CELL SURVIVAL; DOSE RESPONSE; DRUG ANTAGONISM; DRUG EFFECT; ENDOPLASMIC RETICULUM; ENZYMOLOGY; HOMEOSTASIS; MALE; METABOLISM; PATHOLOGY; PHOSPHORYLATION; PHYSIOLOGICAL STRESS; PROSTATE TUMOR; TIME; TUMOR CELL LINE;

ANTINEOPLASTIC AGENTS; APOPTOSIS; CALCIUM; CALPAIN; CASPASES; CELL LINE, TUMOR; CELL SURVIVAL; CHELATING AGENTS; DOSE-RESPONSE RELATIONSHIP, DRUG; ENDOPLASMIC RETICULUM; ENZYME ACTIVATION; ENZYME INHIBITORS; HOMEOSTASIS; HUMANS; MALE; MITOGEN-ACTIVATED PROTEIN KINASES; NAD(P)H DEHYDROGENASE (QUINONE); NAPHTHOQUINONES; PHOSPHORYLATION; PROSTATIC NEOPLASMS; SIGNAL TRANSDUCTION; STRESS, PHYSIOLOGICAL; TIME FACTORS;

EID: 58149140268     PISSN: 02133911     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

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