Cx(3)Cl1 Promotes Tumour Cell By Inducing Tyrosine Phosphorylation Of Cortactin In Lung Cancer

It has been reported that chemokine CX(3)CL1 can regulate various tumours by binding to its unique receptor CX(3)CR1. However, the effect of CX(3)CL1-CX(3)CR1 on the lung adenocarcinoma and lung squamous cell carcinoma is still unclear. Here, we showed that CX(3)CL1 can further invasion and migration of lung adenocarcinoma A549 and lung squamous cell carcinoma H520. In addition, Western blot and immunofluorescence test indicated CX(3)CL1 up-regulated the phosphorylation level of cortactin, which is a marker of cell pseudopodium. Meanwhile, the phosphorylation levels of c-Src and c-Abl, which are closely related to the regulation of cortactin phosphorylation, are elevated. Nevertheless, the src/abl inhibitor bosutinib and mutations of cortactin phosphorylation site could inhibit the promotion effect of CX(3)CL1 on invasion and migration of A549 and H520. Moreover, these results of MTT, Hoechst staining and Western blot suggested that CX(3)CL1 had no effect on the proliferation and apoptosis of A549 and H520 in vitro. The effects of CX(3)CL1 were also verified by the subcutaneous tumour formation in nude mice, which showed that it could promote proliferation and invasion of A549 in vivo. In summary, our results indicated that CX(3)CL1 furthered invasion and migration in lung cancer cells partly via activating cortactin, and CX(3)CL1 may be a potential molecule in regulating the migration and invasion of lung cancer.