Anticancer research, 2005-03, Vol.25 (2A), p.971-979
2005
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Details
- Autor(en) / Beteiligte
- Titel
- Ellagic Acid Induced p53/p21 Expression, G1 Arrest and Apoptosis in Human Bladder Cancer T24 Cells
- Ist Teil von
- Anticancer research, 2005-03, Vol.25 (2A), p.971-979
- Ort / Verlag
- Attiki: International Institute of Anticancer Research
- Erscheinungsjahr
- 2005
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- It is well known that dietary phenolic compounds can elicit vital cellular responses such as cytotoxicity, cell cycle arrest and apoptosis by activating a cascade of molecular events. Ellagic acid is one of these phenolic compounds, but the exact mechanism of its action is still unclear. The objective of this study was to investigate ellagic acid-induced cell cycle arrest and apoptosis in T24 human bladder cancer cells in vitro. Assays were performed to determine cell viability, cell cycle arrest, apoptosis, caspases-3 activity and gene expression, measured by flow cytometric assay, polymerase chain reaction (PCR) and determination of caspase-3 activity. Ellagic acid significantly reduced the viable cells, induced G0/G1-phase arrest of the cell cycle and apoptosis. Ellagic acid also increased p53 and p21 and decreased CDK2 gene expression, that may lead to the G0/G1 arrest of T24 cells. Ellagic acid also promoted caspase-3 activity after exposure for 1, 3, 6, 12 and 24 h, which led to induction of apoptosis. Furthermore, the ellagic acid-induced apoptosis on T24 cells was blocked by the broad-spectrum caspase inhibitor (z-VAD-fmk).
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0250-7005eISSN: 1791-7530Titel-ID: cdi_proquest_miscellaneous_67790634
- Format
- –
- Schlagworte
- Aged, Aged, 80 and over, Amino Acid Chloromethyl Ketones - pharmacology, Apoptosis - drug effects, Apoptosis - physiology, Biological and medical sciences, Caspase 3, Caspase Inhibitors, Caspases - metabolism, CDC2-CDC28 Kinases - biosynthesis, CDC2-CDC28 Kinases - genetics, Cell Cycle Proteins - biosynthesis, Cell Cycle Proteins - genetics, Cell Line, Tumor, Cyclin-Dependent Kinase 2, Cyclin-Dependent Kinase Inhibitor p21, Dose-Response Relationship, Drug, Ellagic Acid - pharmacology, Enzyme Activation - drug effects, Female, G1 Phase - drug effects, Gene Expression - drug effects, Humans, Medical sciences, Nephrology. Urinary tract diseases, RNA, Messenger - biosynthesis, RNA, Messenger - genetics, Tumor Suppressor Protein p53 - biosynthesis, Tumor Suppressor Protein p53 - genetics, Tumors, Urinary Bladder Neoplasms - drug therapy, Urinary Bladder Neoplasms - genetics, Urinary Bladder Neoplasms - metabolism, Urinary Bladder Neoplasms - pathology, Urinary system involvement in other diseases. Miscellaneous, Urinary tract. Prostate gland