Benzo(a)pyrene promotes Hep-G2 cell migration and invasion by upregulating phosphorylated extracellular signal-regulated kinase expression.

Benzo(a)pyrene (BaP), a carcinogenic component of cigarette smoke, has been reported to activate extracellular signal-regulated kinase (ERK) in cancer cells. Furthermore, activated ERK is associated with liver cancer cell invasion and metastasis. Therefore, the aim of the present study was to investigate the potential role of phosphorylated (p)-ERK in BaP-induced Hep-G2 cell migration and invasion. An MTT assay was used to determine the effects of BaP treatment on Hep-G2 cell proliferation. Wound-healing and Transwell invasion assays were employed to assess the migration and invasion abilities of Hep-G2 cells. Western blot analysis was applied to detect the expression of proteins. The results of the present study demonstrated that BaP treatment was able to increase the level of p-ERK protein expression in Hep-G2 cells. BaP treatment promoted Hep-G2 cell migration and invasion. The ERK inhibitor, U0126, was able to block the migration and invasion abilities of Hep-G2 cells induced by BaP. The results of the present study demonstrated that BaP treatment promoted the migration and invasion of Hep-G2 cells by upregulating p-ERK expression.