ObjectiveTo investigate the inhibitory effect of heat shock protein 90 (HSP90) inhibitors of 17-propylene amino-17-demethoxy geldanamycin (17-AAG) combining with paclitaxel on human anaplastic thyroid cancer FRO cell line. Method①The proliferation inhibition rates of FRO cells were detected by mmethyl thiazolyl tetrazolium (MTT) assay in different concentration groups (17-AAG: 0.312 5, 0.625 0, 1.2500, 2.5000, and 5.0000 μmol/L; paclitaxel: 0.001 0, 0.0100, 0.1000, and 1.0000 μmol/L; combination group, 17-AAG: 0.625 0 μmol/L, paclitaxel: 0.001 0, 0.0100, 0.1000, and 1.0000 μmol/L) and at different time points (24, 48, and 72 hours). ②The change of cell cycle and apoptosis rates of FRO cells were detected in 17-AAG group (0.625 0 μmol/L), paclitaxel group (0.1000 μmol/L), and combination group (17-AAG: 0.625 0 μmol/L, paclitaxel: 0.1000 μmol/L) by flow cytometry at 24 hours after treatment. ③activity of Caspase-3 and Caspase-9 in FRO cells of 17-AAG group (0.625 0 μmol/L), paclitaxel group (0.1000 μmol/L), and combination group (17-AAG: 0.625 0 μmol/L, paclitaxel: 0.1000 μmol/L) was detected by Caspase-3 detection reagent box and Caspase-9 detection reagent box respectively. FRO cells of normal control group were treated without any drug, but culture solution. Results①The proliferation inhibition rates of FRO cells increased with the increase of concentra-tion (17-AAG, paclitaxel, combination of 17-AAG and paclitaxel), there was significant difference between any 2 groups (normal control group included), P<0.05. In addition, the proliferation inhibition rates of FRO cells in any concentration group (normal control group excluded) increased over time (24, 48, and 72 hours), there was significant difference between any 2 time points (P<0.05). The proliferation inhibition rates of FRO cells in combination group were all higher than those of 17-AAG group and paclitaxel group in condition of same time point and same concentration (P<0.05). The q value of combination group was higher than 1.15 at 3 time points in all concentration, that meant 17-AAG could increase the efficiency of paclitaxel. ②The apoptosis rate of FRO cells in normal control group was lower than those of 17-AAG group, paclitaxel group, and combination group (P<0.05), and apoptosis rate of FRO cells in combination group was higher than those of 17-AAG group and paclitaxel group (P<0.05). ③Activity of Caspase-3 and Caspase-9 of FRO cells in normal control group were lower than those of 17-AAG group, paclitaxel group, and combination group (P<0.05), and activity of Caspase-3 and Caspase-9 of FRO cells in combination group were higher than those of 17-AAG group and paclitaxel group (P<0.05). Conclusions17-AAG and paclitaxel can significantly inhibit the proliferation and induce the apoptosis of FRO cells. The combination of the two kinds of drugs may generate synergy, with dose-dependence effect.