Induction of mitotic arrest and apoptosis in human prostate cancer PC-3 cells by evodiamine
Journal
Journal of Urology
Journal Volume
173
Journal Issue
1
Pages
256-261
Date Issued
2005
Author(s)
Abstract
Purpose: Although evodiamine, an alkaloid isolated from Evodiae fructus, has been reported to exert anticancer activities, to our knowledge its target and mechanism of action have not yet been explored. We examined the anticancer activities and action mechanism of evodiamine. Materials and Methods: Human prostate cancer PC-3 cells were used in this study. The cytotoxic effect and cell growth inhibition were examined using the MTT (3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide) assay and sulforhodamine B assay, respectively. The apoptotic effect was determined using TUNEL assay and the progression of cells through the cell cycle and cell apoptosis were examined by FACScan flow cytometry (Becton Dickinson, Sunnyvale, California). In situ mitotic spindle detection and in vitro tubulin polymerization assay were performed by immunofluorescence staining for β-tubulin and CytoDYNAMIX ScreenTM3 (CDS-03) kits (Cytoskeleton, Denver, Colorado). Results: It was found that treatment of PC-3 cells with evodiamine decreased the cell number in a concentration and time dependent manner, and effectively inhibited PC-3 cell growth via the induction of cell cycle arrest at the G2/M phase and subsequent apoptosis. In an in situ assay we found that evodiamine inhibited microtubule spindle formation. In a cell-free assay system of tubulin polymerization evodiamine inhibited the polymerization of microtubules in a concentration dependent manner. Conclusions: These data suggest that evodiamine shows anticancer activity through inhibition of tubulin polymerization. This antitubulin activity might make evodiamine a potential anticancer drug.
SDGs
Other Subjects
3 (4,5 dimethyl 2 thiazolyl) 2,5 diphenyltetrazolium bromide; antineoplastic agent; beta tubulin; evodiamine; sulforhodamine B; antineoplastic activity; apoptosis; article; cell count; cell cycle; cell growth; concentration response; controlled study; cytotoxicity; device; disease course; drug mechanism; growth inhibition; human; human cell; human tissue; immunofluorescence; microtubule assembly; mitosis inhibition; mitosis spindle; nick end labeling; priority journal; prostate cancer
Publisher
Lippincott Williams and Wilkins
Type
journal article