Table 3. A-803467 cannot enhance the cytotoxicity of ABCB1 and ABCC10 substrate anticancer agents in HEK293/PCDNA3.1 cells overexpressing ABCB1 and ABCC10.
| Treatments | IC50 ± SD (nM) | |||||
|---|---|---|---|---|---|---|
| HEK293/pc DNA3.1 | FR | HEK293/ABCB1 | RF | HEK293/ABCC10 | FR | |
| Paclitaxel | 8.3 ± 0.2 | 1.0 | 525.2 ± 20.1 | 63.2# | 95.2 ± 6.1 | 11.4# |
| +A-803467 (7.5 μM) | 7.9 ± 0.4 | 0.9 | 453 ± 18.9 | 54.5 | 77.4 ± 5.6 | 9.3 |
| +Verapamil (5 μM) | 8.2 ± 0.6 | 1.0 | 9.5 ± 1.5 | 1.0 * | − | − |
| +Cepharanthine (2.5 μM) | 7.2 ± 0.3 | 0.8 | − | − | 12.3 ± 2.5 | 1.4* |
Data represents the mean IC50 values for each cell line ± SD obtained from three independent sets of experiments. Statistical analysis was performed by One-way ANOVA followed by Newman-Keuls Multiple Comparison Test. Statistical significance was set at P < 0.05.
*
P < 0.05 versus the control group.
#
P < 0.05 versus the control of HEK293/pcDNA3.1 group.
The fold resistance (FR) was determined by dividing the IC50 value of the anticancer drug for HEK293/pcDNA3.1, HEK293/ABCB1 and HEK293/ABCC10, in the absence or presence of reversal agents, by the IC50 value of the respective anticancer drug for HEK293/pcDNA3.1 in the absence of reversal agent. Verapamil and cepharanthine were used as positive control inhibitors for ABCB1 and ABCC10 respectively.