The flavonoid Casticin has multiple mechanisms of tumor cytotoxicity action
| Autor: | Khadidja Haidara, Lolita Zamir, Gerald Batist, Qui-Wen Shi |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Cyclin-Dependent Kinase Inhibitor p21
Cancer Research Tetrazolium Salts Antineoplastic Agents Apoptosis Biology chemistry.chemical_compound Cell Line Tumor Neoplasms CDC2 Protein Kinase Humans Cell Proliferation Flavonoids Cyclin-dependent kinase 1 Dose-Response Relationship Drug Cell growth Plant Extracts Cell Cycle Cell cycle Cell biology Thiazoles Cell killing Oncology chemistry Models Chemical Cell culture Cancer cell Mutation Casticin Cancer research |
| Zdroj: | Cancer letters. 242(2) |
| ISSN: | 0304-3835 |
| Popis: | We studied the mechanism of anti-tumor activity of the flavonoid Casticin, derived from Achillea millefolium. Casticin anti-tumor activity results in cell growth arrest in G2/M and in apoptotic death. As a tubulin-binding agent (TBA), Casticin induces p21, which in turn inhibits Cdk1. Moreover, Casticin appears to down regulate cyclin A. These observations could explain Casticin-induced G2/M arrest. Following Casticin exposure, Bcl-2 depletion occurs in cancer cells, and a sub-G1 accumulation occurs in the cell cycle. Moreover, following a transient transfection with Bcl-2, MN1 cells are resistant to Casticin. A number of features suggest that Casticin could be important in cancer therapy. Indeed, Pgp over expressing cells are not resistant to Casticin, and its cell killing effect is observed even in p53 mutant or null cell lines. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect