Abstract
Cadmium (Cd) is an established carcinogen that is involved in the progression of lung cancer. However, the mechanisms underlying this Cd-induced process have yet to be fully elucidated. The present study explored the potential roles of phosphorylated (p)-ERK in the Cd-induced migration and invasion of lung cancer cells. An MTT assay was performed to evaluate cell viability whilst western blot analysis and reverse transcription-quantitative PCR were used to detect the expression of protein and mRNA, respectively. Migration and invasion assays were performed to assess cell migratory and invasive abilities. The results demonstrated that exposure to Cd increased the expression of p-ERK in A549 cells. Cd also enhanced the migration and invasion of A549 cells, which could be blocked via U0126 treatment (an inhibitor of mitogen activated protein kinase). In addition, it was identified that Cd-induced expression of matrix metalloproteinases 2 mRNA was mediated by p-ERK. In conclusion, the present findings indicated that Cd induced A549 cell migration and invasion by activating ERK, and it was hypothesized that p-ERK could serve as a target in the clinical treatment of Cd-induced lung cancer.