Atmospheric particulate matter(2.5) promotes the migration and invasion of hepatocellular carcinoma cells

Epidemiological data has demonstrated that particulate matter (PM) with an aerodynamic diameter ≤ 2.5 µm (PM(2.5)) is associated with cancer incidence. However, the precise mechanisms underlying PM(2.5)-mediated hepatocellular carcinoma cancer (HCC) migration and invasion remain unclear. The aim of the present study was to explore the response of the HCC cell lines HepG2 and HuH-7 to PM(2.5) exposure. The results revealed that PM(2.5) treatment promoted the migration and invasion of HCC cells, in addition to increasing protein levels of matrix metalloproteinase (MMP)-13. Additionally, PM(2.5) induced intracellular reactive oxygen species formation in HCC cells. Further investigation revealed that phosphorylation of RAC-alpha serine/threonine-protein kinase (AKT) increased in response to PM(2.5) exposure in HCC cells, and the AKT antagonist LY294002 reduced PM(2.5)-induced migration, invasion and MMP-13 expression. In addition, the data from the present study demonstrated that high concentrations of PM(2.5) decreased the proliferation of normal HL7702 hepatocyte cells and promoted apoptosis. These results indicate that the activation of AKT by PM(2.5) results in MMP-13 overexpression, and stimulates HCC cell migration and invasion. In conclusion, the results from the present study demonstrate that PM(2.5) promotes HCC development and elucidate a potential underlying molecular mechanism for this effect.