Ezrin promote esophageal cancer cell migration and other biological behavior

Ezrin belongs to ERM family, is a membrane protein actin cytoskeleton and cell connections between those who, in the maintenance of cell shape and regulation of intracellular signal transduction process plays a very important function. Our group had previously found that immortalized esophageal epithelial cells in malignant transformation, Ezrin significantly abnormal overexpression and knock down ezrin gene expression can inhibit the movement of esophageal cancer cell invasion. The test results showed that clinical esophageal carcinoma, Ezrin overexpression with patient survival was significantly negatively correlated; Description Ezrin cautionary prognostic role of esophageal cancer, is an important molecular markers. The basis of the above research, the paper proposed by mutation sites of key amino acid residues, namely threonine 567, combined with antisense blocking experiments, Ezrin promote further explored the molecular mechanisms of esophageal cancer cell migration. First, the three mutations ezrin plasmids, including pEGFP-N1-ezrin-T / A (T567A), pEGFP-N1-ezrin-T / D (T567D), pEGFP-N1-ezrin-Nter (N terminal truncated, 309aa), and pEGFP-N1-ezrin-wt (wild type) cells were transfected esophageal EC109, thereby detecting the movement ability of cells in each group changes. The results found that cells transfected with empty vector (pEGFP-N1) cells compared to the control group, 1) transfected with pEGFP-N1-ezrin-T / D plasmid esophageal cancer cells the ability to move significantly enhanced; 2) transfected with pEGFP-N1 -ezrin-T / A and pEGFP-N1-ezrin-wt of esophageal cancer cells showed no significant change in the ability to move; 3) transfected with pEGFP-N1-ezrin-Nter of esophageal cancer cells the ability to move significantly. This indicates that threonine residue 567 locus with Ezrin is essential to promote mobility of esophageal cancer cells, it may point to the location-related phosphorylation. Secondly, the detection of the proliferation of cells in each group changes. The results found that cells transfected with empty vector (pEGFP-N1) cells compared to the control group, 1) transfected with pEGFP-N1-ezrin-T / D of esophageal cancer cell proliferation has significantly enhanced, 2) were transfected with pEGFP- N1-ezrin-T / A, pEGFP-N1-ezrin-Nter and pEGFP-N1-ezrin-wt esophageal cancer cell proliferation did not change significantly. Finally, the detection of the cell cycle in each group. The results found that cells transfected with empty vector (pEGFP-N1) compared a control group of cells transfected with pEGFP-N1-ezrin-T / A and pEGFP-N1-ezrin-Nter esophageal cancer cells were arrested in the G1 phase, transfer stained transfected pEGFP-N1-ezrin-wt esophageal cancer cells were arrested in S phase, transfection transfected pEGFP-N1-ezrin-T / D of esophageal cancer cells were arrested at G2 / M phase. In summary visible, Ezrin promote the role of esophageal cancer cells move to its present point of 567 C-terminal threonine close, but may also involve the phosphorylation site machining and other processes.