Aims: The purpose of our study was to explore the combination effect of epirubicin and Bacillus
Calmette Guerin (BCG) and its mechanism.
Background: Bladder cancer is a threat to human health worldwide. Commonly used chemotherapy drugs and
biotherapy have significant therapeutic effects on bladder cancer, but the mechanism and combined effects are
Objective: To evaluate the anti-cancer effect of epirubicin combined with BCG on human bladder cancer cells,
our studies were carried out.
Methods: The viability of human bladder cancer cells with epirubicin and/or BCG treatments was examined by
Cell Counting Kit-8 (CCK-8) assay. Apoptosis and cell cycle phase were determined by flow cytometry analysis.
Pre-apoptosis factors of caspase-3, p53, B-cell lymphoma 2 associated X protein (Bax) and anti-apoptosis
factor of B-cell lymphoma 2 (Bcl-2) were detected by western blot.
Results: The viability of human bladder cancer with epirubicin or BCG treatment was decreased and the viability
with epirubicin combined with BCG treatment was decreased more, which were determined by CCK-8
assay. Both epirubicin and BCG increased the apoptosis rate of human bladder cancer and arrested more cells
into G0/G1 phase, which were tested by flow cytometry. The expression of caspase-3, p53 and Bax was increased
and the expression of Bcl-2 was decreased with epirubicin treatment on human bladder cells, which
were analyzed by western blot. The expression of caspase-3 and p53 was increased with BCG treatment, which
was examined by western blot.
Conclusion: Epirubicin induced apoptosis in human bladder cancer cells by up-regulating the expression of proapoptotic
factors (caspase-3, p53 and Bax) and down-regulating the expression of anti-apoptotic factor (Bcl-2).
BCG promoted apoptosis of human bladder cancer cells by up-regulating the expression of caspase-3 and p53.
BCG plays a potential role at the time of the combination of epirubicin and BCG on bladder cancer cells in early
stage. Both epirubicin and BCG affected cell cycle distribution via arresting more bladder cancer cells at G0/G1
phase, which ultimately led bladder cancer proliferation in vitro and promoted apoptosis.