Fig. 4

A MRE11 knockdown led to decreased RUNX2 expression, while MRE11 overexpression led to increased RUNX2 expression, in oral cancer cells. B The correlation of RUNX2 expression in oral cancer tissues with MRE11 expression and lymph node metastasis in oral cancer patients. C A positive correlation between RUNX2 and CXCR4 expression in oral cancer tissues. D CXCR4 expression in oral cancer cells was decreased when MRE11 was knockdowned. E MRE11 and CXCR4 were positively correlated in primary oral cancer tissues and CXCR4 was more highly expressed in oral cancer tissues with lymph node metastasis. F MRE11 knockdown led to decreased pAKT expression, while MRE11 overexpression led to increased pAKT expression, in oral cancer cells. G The correlation between MRE11 and pAKT expression in oral cancer tissues. H Wortmannin, a PI3K/AKT inhibitor, reversed the increased oral cancer migration induced by MRE11 overexpression. I CXCR4 silencing reversed the increased pAKT expression caused by MRE11 overexpression. J CXCR4 blocking mAb reversed the increased pAKT expression caused by SDF-1, a CXCR4 activator, in MRE11-overexpressing oral cancer cells. K MRE11 knockdown in oral cancer cells led to increased expression of nuclear FOXA2, which was partially reversed by cotreatment with AKT activator SC79. L MRE11 overexpression in oral cancer cells decreased the nuclear expression of FOXA2 while treatment with wortmannin reversed the increased nuclear expression of FOXA2 induced by MRE11 overexpression. M Correlation of MRE11 and FOXA2 expression in oral cancer tissues and metastatic lymph nodes. N Correlation of phospho-AKT and FOXA2 expression in oral cancer tissues and metastatic lymph nodes.