Objective To investigate the inhibitory effects of disulfiram combined with paclitaxel on the proliferation and invasion of esophageal cancer cells and their mechanism.Methods The esophageal cancer cell lines TE-1 and TE-10 were treated with different concentrations of disulfiram(0,10,20,40 μmol/L),and the cell viability was measured by CCK-8 method to screen the optimal concentration of disulfiram.The intervention concentration of disulfiram was 20 μmol/L.TE-1 and TE-10 esophageal cancer cells were divided into the control group(normal culture without drugs),di-sulfiram group(20 μmol/L disulfiram),paclitaxel group(0.5 μmol/L paclitaxel),disulfiram + paclitaxel group(20 μmol/L disulfiram +0.5 μmol/L paclitaxel),respectively.MTT assay was used to observe the cell proliferation,flow cy-tometry was used to observe the apoptosis rate,Transwell assay was used to observe the cell invasion ability,RT-qPCR was used to detect the mRNA of α-tubulin,and Western blotting was used to detect the protein expression levels of α-tubulin and B-cell lymphoma-2(Bcl-2).Results The proliferation rates of TE-1 and TE-10 cells were in the following order:control group>disulfiram group>paclitaxel group>disulfiram + paclitaxel group,apoptosis rates of TE-1 and TE-10 cells were as follows:control group<disulfiram group<paclitaxel group<disulfiram + paclitaxel group,the number of trans-membrane TE-1 and TE-10 cells was as follows:control group>disulfiram group>paclitaxel group>disulfiram + paclitax-el group,the expression of α-tubulin mRNA in TE-1 cells was as follows:control group>disulfiram group>paclitaxel group>disulfiram + paclitaxel group,the expression of α-tubulin mRNA in TE-10 cells was in the following order:control group>disulfiram group>paclitaxel group,disulfiram + paclitaxel group,and the expression levels of α-tubulin and Bcl-2 protein in TE-1 and TE-10 cells were as follows:control group>disulfiram group>paclitaxel group>disulfiram + pacli-taxel group(all P<0.05).Conclusion Disulfiram combined with paclitaxel may enhance the inhibitory effects on the proliferation and invasion of esophageal cancer cells probably by down-regulating tubulin and promoting apoptosis.
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