Abstract
Icotinib is an epidermal growth factor receptor tyrosine kinase inhibitor, which has been revealed to inhibit proliferation in tumor cells. However, the effect of icotinib on cancer cell metastasis remains to be explained. This study examines the effect of icotinib on the migration and invasion of squamous cells of tongue carcinoma (Tca8113 cells) in vitro. The results of the Boyden chamber invasion assay demonstrated that icotinib reduced cell invasion, suppressed the protein levels of matrix metalloproteinases (MMPs), MMP-2 and MMP-9, and increased the expression of tissue inhibitor of metalloproteinase-1. In addition, icotinib was found to significantly decrease the protein levels of nuclear factor κB (NF-κB) p65, which suggested that icotinib inhibits NF-κB activity. Furthermore, treatment with the NF-κB inhibitor, pyrrolidine dithiocarbamate, suppressed cell invasion and MMP-2 expression. These results suggested that icotinib inhibits the invasion of Tca8113 cells by downregulating MMP via the inactivation of the NF-κB signaling pathways.
Highlights
Studies have shown that the matrix metalloproteinases (MMPs), including MMP‐2 and MMP‐9, are key proteases in the invasion and metastasis of human oral squamous carcinoma and breast cancer cells [1,2]
Anti‐human MMP2, MMP9, TIMP1 and TIMP2 antibodies were purchased from Cell Signaling Technology, Inc. (Danvers, MA, USA), while rabbit polyclonal anti‐human nuclear factor κB (NF‐κB) p65 antibody was purchased from Millipore (Billerica, MA, USA) and mouse monoclonal anti‐ox histone H1 was purchased from Millipore (Bedford, MA, USA)
The results demonstrated that icotinib reduced the invasion of Tca8113 cells in a concentration‐dependent manner when treated with 0, 0.5, 1 and 2 μM of icotinib for 24 h (Fig. 2)
Summary
Studies have shown that the matrix metalloproteinases (MMPs), including MMP‐2 and MMP‐9, are key proteases in the invasion and metastasis of human oral squamous carcinoma and breast cancer cells [1,2]. TIMP‐1 and TIMP‐2 have the ability to inhibit tumor invasion and metastasis [3]. It has been reported that follicle‐stimulating hormone affects the proliferation and invasion of ovarian cancer cells by regulating the NF‐κB signaling pathway [6]. Inhibition of the NF‐κB pathway may potentially prevent proliferation and invasion in a broader range of tumors. The NF‐κB signaling pathways are significant in regulating the expression of MMPs. The stilbenoid, piceatannol, suppresses breast cancer cell invasion through the inhibition of NF‐κB pathways [7]. The NF‐κB pathways are potential targets for the treatment of tumors
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