CXCR4 has been reported in various types of human
cancer, which is associated with
cancer progression and
metastasis. However, the investigation of CXCR4 in
laryngeal cancer is extremely rare. In the present study, we used lentivirus-mediated
shRNA targeting CXCR4 to silenced CXCR4 expression in Hep-2 cells and evaluated the effect of long-term suppression of CXCR4 on Hep-2 growth and
metastasis. The Cell proliferation was analyzed by MTS assay, and the invasion and
metastasis potentials were analyzed using wound healing and transwell assays, respectively. Our results showed that lentivirus-mediated
shRNA effectively infected Hep-2 cells and suppressed CXCR4 expression, and inhibited cell growth of Hep-2 cells. Cell invasion and apoptosis were decreased concomitantly with the reduction in CXCR4
protein expression. Further analysis revealed that CXCR4 silencing caused the reducion of CXCR4, CXCL12, TIMP2,
VEGF and MMP9, and the phosphorylation levels of IκB, AKT and MAPK, and also decreased the activity of NF-κB. These results suggested that knockdown of CXCR4 inhibits the invasion and
metastasis of Hep-2 through PI3K/AKT and MAPK signaling pathways, by decreasing NF-κB activities to down-regulate
VEGF,
TIMP-2 and MMP-9 expression. These data demonstrate that the inhibition of CXCR4 may be an effective interventional therapeutic strategy in
laryngeal cancer.