Epidemiological studies have demonstrated a close correlation between
nickel exposure and the incidence of
lung cancer. Several studies have suggested that
nickel contributes to
tumor progression of human
lung cancer. In this in vitro study, we found that
nickel, as
nickel chloride, could significantly enhance the invasive potential of human
lung cancer cells, accompanied by elevated expression of
IL-8, TGF-β, MMP2 and MMP9 in human
lung cancer cells. Importantly, we demonstrated that
nickel could activate TLR4 signaling in human
lung cancer cells. Further studies showed that the TLR4/MyD88 signaling conferred the enhanced invasive potential of human
lung cancer cells induced by
nickel. Finally, we revealed that the p38MAPK pathway and
NF-kB pathway were necessary for the enhanced invasive potential of human
lung cancer cells induced by
nickel. Our data provide a mechanistic explanation for
nickel induced invasion of human
lung cancer, and they suggest new strategies for
nickel-related
lung cancer clinical
biotherapies.