Effect of dorsomorphin on the migration and invasion abilities of drug-resistant esophageal cancer cells

Objective To investigate the effect of dorsomorphin, a bone morphogenetic protein (BMP) small-molecule inhibitor, on the migration and invasion abilities of drug-resistant esophageal cancer EC109/PTX cells. Methods MTT assay was used to observe the effect of different concentrations of dorsomorphin on the proliferation of EC109/PTX cells and determine the concentration for subsequent experiments. Dorsomorphin at the concentration of 1 μmol/L was established as the experimental group, and a blank control group was set up. EC109/PTX cells were treated for 48 h. Flow cytometry was used to observe the effect of dorsomorphin on the apoptosis of EC109/PTX cells; scratch assay and Transwell assay were used to observe the migration and invasion abilities of EC109/PTX cells; Western blotting was used to measure the relative protein expression levels of Vimentin, E-cadherin, and N-cadherin in EC109/PTX cells. Results Dorsomorphin at the concentration of 1 μmol/L showed an inhibition rate of (9.89±1.12)% on the proliferation of EC109/PTX cells. At 48 h of culture, there was no significant difference in the apoptosis rate of EC109/PTX cells between the control group and the experimental group (P>0.05). Scratch assay and Transwell assay showed that compared with the control group, the experimental group had significant reductions in the migration rate and cell permeation rate of EC109/PTX cells (t=85.42,19.65,P<0.05). Western blotting showed that compared with the control group, the experimental group had significant reductions in the relative protein expression levels of Vimentin and N-cadherin (t=19.40,41.79,P<0.05) and a significant increase in the protein expression level of N-cadherin (t=58.12,P<0.05). Conclusion The BMP inhibitor dorsomorphin can inhibit the migration and invasion abilities of drug-resistant tumor cells by affecting the expression of epithelial-mesenchymal transition-related proteins in drug-resistant esophageal cancer cells.