This study demonstrates that two anticancer drugs,
taxol and
doxorubicin (Dox), can kill human
hepatoblastoma HepG2 cells in a dose-dependent manner via the induction of apoptosis. Characteristic events, including externalization of
phosphatidylserine, cytoplasmic shrinkage,
chromatin condensation and
DNA degradation, were observed in a large majority of the
drug-treated cells. DNA fragmentation showed that a ladder of
DNA fragments of approximately 200 bp multiples was observed in
taxol-treated, but not in Dox-treated, cells. In addition, the expression patterns of Bcl-2 family members during
taxol or Dox treatment were investigated. Results from Western blot analysis indicated that HepG2 cells did not express either the death repressor Bcl-2, or the death promoters Bcl-XS and Bax. However, during the apoptotic process one death repressor, Bcl-XL, and two death promoters, Bak and Bad, were expressed. The expression levels of Bcl-XL and Bak remained unchanged, whereas the level of Bad was down-regulated. As the ratio between death repressors and death promoters in the Bcl-2 family will determine the sensitivity of cells to apoptotic stimuli, the findings suggest that the changed expression patterns of Bcl-2 family
proteins caused by anticancer drugs in
liver cancer cells may be involved in chemoresistance.