(-)-Epigallocatechin-3-gallate inhibits osteosarcoma cell invasiveness by inhibiting the MEK/ERK signaling pathway in human osteosarcoma cells.

The notorious lung metastatic capability of osteosarcoma aggravates patient mortality and remains the primary challenge to be overcome. We investigated the effect of (-)-epigallocatechin-3-gallate (EGCG) on the metastasis capability of osteosarcoma cells. We performed cytotoxicity assays (MTT) to determine the appropriate concentration of EGCG for experiments. Migration, invasion, wound-healing, and adhesion assays were performed to assess the effect of EGCG on the metastasis of osteosarcoma. Changes in the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway were investigated using Western blot analyses. In addition, a MEK inhibitor (U0126) was used in invasion assays to determine the effect of the MEK/ERK signaling pathway. We found that EGCG may markedly inhibit the migration and invasion capacity of osteosarcoma cells, which occurred concurrently with inhibition of the expression of phospho-MEK and phospho-ERK. Inhibitors of MEK inhibited the invasion of osteosarcoma cells, and this effect could be enhanced by EGCG. We also detected the expression of c-Jun N-terminal kinase, p38, and their respective phospho-proteins, but did not find any meaningful changes. Taken together, our results demonstrated that EGCG could inhibit the metastasis capability of osteosarcoma cells by inhibiting MEK/ERK signaling activity and may provide new therapeutic value for osteosarcoma.