Τίτλος:
Ursolic acid triggers apoptosis and Bcl-2 downregulation in MCF-7 breast cancer cells
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
In this report we determine the ability of ursolic acid (UA) to induce apoptosis and to modulate glucocorticoid receptor (GR) and Activator Protein-1 (AP-1) in MCF-7 cells. The UA-induced apoptosis (53 μM), the PARP cleavage, and the decrease in Bcl-2 protein (53 μM) support the notion that UA induces apoptosis through the intrinsic mitochondrial pathway. UA binds GR (relative binding affinity: 2.57) and translocates GR into nucleus, suggesting its potential as a GR modulator. UA had no effect on GRE- or TRE-driven gene expression. In summary, UA is a GR modulator and may be considered as a potential anticancer agent in breast cancer. Copyright © Informa Healthcare USA, Inc.
Συγγραφείς:
Kassi, E.
Sourlingas, T.G.
Spiliotaki, M.
Papoutsi, Z.
Pratsinis, H.
Aligiannis, N.
Moutsatsou, P.
Περιοδικό:
Cancer Investigation
Λέξεις-κλειδιά:
caspase 3; caspase 7; caspase activated deoxyribonuclease; dexamethasone; DFF45 protein; glucocorticoid receptor; luciferase; mifepristone; nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase; protein bcl 2; transcription factor AP 1; triamcinolone; unclassified drug; ursolic acid, apoptosis; article; breast cancer; cell nucleus; cell strain MCF 7; cell viability; controlled study; drug cytotoxicity; drug isolation; flow cytometry; gel mobility shift assay; gene expression; genetic transfection; HeLa cell; human; human cell; mitochondrion; priority journal; protein cleavage; protein DNA binding; Salvia officinalis; transcription regulation; Western blotting, Active Transport, Cell Nucleus; Adenocarcinoma; Antineoplastic Agents; Apoptosis; Binding, Competitive; Breast Neoplasms; Cell Line, Tumor; Dexamethasone; Down-Regulation; Drug Screening Assays, Antitumor; Female; Gene Expression Regulation, Neoplastic; Genes, bcl-2; Hela Cells; Humans; Mifepristone; Neoplasm Proteins; Poly(ADP-ribose) Polymerases; Proto-Oncogene Proteins c-bcl-2; Receptors, Glucocorticoid; Transcription Factor AP-1; Transcription, Genetic; Triamcinolone; Triterpenes
DOI:
10.1080/07357900802672712
