MECHANISM OF TAXOL-INDUCED APOPTOSIS IN HUMAN BREAST CANCER CELLS
Abstract
Objective: To investigate the mechanism by which taxol induces apoptosis in human breast cancer cells.
Methods: Cell morphology, agarose gel electrophores, flow cytometry, video time-lapse monitor and Western blot were performed for investigating taxol-induced apoptosis in human breast cancer cells (BCap 37).
Results: BCap 37 cells treated with taxol (100 nm) underwent the arrests of cell mitosis at metaphase of mitosis and induction of apoptosis. Apoptotic cells demonstrated cell shrinkage, condensation or fragmentation of chromosomes. Nuclear DNA of apoptotic cells displayed ladder bands characteristic of internucleosomal DNA fragmentation. The expression of bcl-2, inhibitor of apotosis, was decreased with modification, while that of bax, inducer of apoptosis, increased only at early stage of the apoptotic pathway and decreased later.
Conclusion: In human breast cancer cells the induction of apoptosis by taxol was closely associated with mitotic arrest of cell cycle, and altered expressions of bcl-2 and bax gene possibly played an important role in regulating taxolinduced apoptosis.
Methods: Cell morphology, agarose gel electrophores, flow cytometry, video time-lapse monitor and Western blot were performed for investigating taxol-induced apoptosis in human breast cancer cells (BCap 37).
Results: BCap 37 cells treated with taxol (100 nm) underwent the arrests of cell mitosis at metaphase of mitosis and induction of apoptosis. Apoptotic cells demonstrated cell shrinkage, condensation or fragmentation of chromosomes. Nuclear DNA of apoptotic cells displayed ladder bands characteristic of internucleosomal DNA fragmentation. The expression of bcl-2, inhibitor of apotosis, was decreased with modification, while that of bax, inducer of apoptosis, increased only at early stage of the apoptotic pathway and decreased later.
Conclusion: In human breast cancer cells the induction of apoptosis by taxol was closely associated with mitotic arrest of cell cycle, and altered expressions of bcl-2 and bax gene possibly played an important role in regulating taxolinduced apoptosis.