The aim of this study was to investigate the mechanism of shikonin (SK) modulation of the vascular endothelial growth factor(VEGF)/extracellular signal-regulated kinase (ERK) signaling pathway affecting epithelial mesenchymal transition (EMT) to inhibit invasion and migration of triple-negative breast cancer(TNBC). The MDA-MB-231 cells of TNBC cell line were used as experimental subjects, and the effect of SK on cell proliferation was assessed by thiazolyl blue tetrazolium bromide (MTT) colorimetric assay, and the inhibitory effect of SK on the migration and invasion ability of TNBC cells was investigated by scratch repair assay and Transwell invasion assay. Western blot (WB) assay was performed to detect the expression of VEGF, ERK1/2 and EMT-associated proteins, including E-cadherin, Vimentin, and Snail. Immunofluorescence assay was performed to detect the effect of SK on the expression of E-cadherin and Vimentin. Compared with the control group (Con), the results showed that SK significantly inhibited the proliferation, migration and invasion of TNBC cells (P<0.05). Compared with the Con group, WB results showed that SK significantly decreased the expression of VEGF, ERK1/2, Vimentin, and Snail (P<0.05) and up-regulated the expression of E-cadherin (P<0.05), and the VEGF-specific inhibitor bevacizumab (Beb) significantly decreased the expression of VEGF and ERK1/2, and the expression of VEGF and ERK1/2 were further downregulated after combinating with SK (P<0.05). Immunofluorescence results showed that the expression of E-cadherin was elevated, and the expression of Vimentin was decreased by the SK. It can be seen that SK inhibited the invasion and migration of triple-negative breast cancer cells by regulating the cellular EMT process through the VEGF/ERK signaling pathway.

shikonin, vascular endothelial growth factor/ extracellular signal-regulated kinase signal pathway, epithelial-mesenchymal transition, triple negative breast cancer, cell invasion; cell migration