MTOR and tongue cancer: AXL knockdown significantly reduced the biochemical levels of p-AKT, p-mTOR and p-NF-ĸB p65 levels and impeded the MMP10-driven proliferation, migration, and invasion phenotypes, whereas AXL overexpression clones restored the p-AKT and p-NF-ĸB p65 levels along with proliferation, migration, and invasion phenotypes of MMP10-knocked down AW8507 cells (Fig. 4b–k), indicating that AXL is downstream of MMP10 and could potentially regulate the ability of tongue cancer cell lines to metastases upon MMP10 upregulation.