Celecoxib inhibits growth of human autosomal dominant polycystic kidney cyst-lining epithelial cells through the VEGF/Raf/MAPK/ERK signaling pathway

Molecular Biology Reports

Volumn 39, Issue 7, 2012, Pages 7743-7753

  Xu, Tao ^a   Wang, Nian Song ^a   Fu, Li Li ^b   Ye, Chao Yang ^b   Yu, Sheng Qiang ^b   Mei, Chang Lin ^b  

^a SHANGHAI JIAO TONG UNIVERSITY AFFILIATED SIXTH PEOPLE S HOSPITAL   (China)

^b SECOND MILITARY MEDICAL UNIVERSITY   (China)

Author keywords

Apoptosis; Autosomal dominant polycystic kidney disease; Celecoxib; COX 2; Proliferation

Indexed keywords

6 OXOPROSTAGLANDIN F1 ALPHA; BROXURIDINE; CASPASE 3; CELECOXIB; CYCLIN A; CYCLIN DEPENDENT KINASE INHIBITOR 1; CYCLINE; CYCLOOXYGENASE 2 INHIBITOR; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN BAX; PROTEIN BCL 2; RAF PROTEIN; THROMBOXANE; VASCULOTROPIN; VASCULOTROPIN RECEPTOR 2;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL CULTURE; CELL CYCLE PROGRESSION; CELL GROWTH; CELL PROLIFERATION; CLINICAL ARTICLE; CONTROLLED STUDY; CREATININE BLOOD LEVEL; DRUG DOSE COMPARISON; DRUG EFFECT; DRUG MECHANISM; DRUG MEGADOSE; ENZYME PHOSPHORYLATION; EPITHELIUM CELL; FIBROSIS; HUMAN; HUMAN CELL; IN VITRO STUDY; IN VIVO STUDY; KIDNEY MASS; KIDNEY POLYCYSTIC DISEASE; MALE; NEUTROPHIL CHEMOTAXIS; NONHUMAN; PROTEIN EXPRESSION; PROTEIN INDUCTION; RAT; RODENT; SIGNAL TRANSDUCTION; UPREGULATION; UREA NITROGEN BLOOD LEVEL;

ANIMALS; APOPTOSIS; BCL-2-ASSOCIATED X PROTEIN; CASPASE 3; CELL CYCLE CHECKPOINTS; CELL PROLIFERATION; CELLS, CULTURED; CYCLIN A; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLOOXYGENASE 2 INHIBITORS; CYSTS; DISEASE MODELS, ANIMAL; EPITHELIAL CELLS; EXTRACELLULAR SIGNAL-REGULATED MAP KINASES; HUMANS; MALE; MAP KINASE SIGNALING SYSTEM; POLYCYSTIC KIDNEY DISEASES; PYRAZOLES; RAF KINASES; RATS; SULFONAMIDES; VASCULAR ENDOTHELIAL GROWTH FACTOR A; VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR-2;

RATTUS; RODENTIA;

EID: 84864288333     PISSN: 03014851     EISSN: 15734978     Source Type: Journal    
DOI: 10.1007/s11033-012-1611-2     Document Type: Article

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