Biological function and regulation mechanism of MTA2 expression in bladder cancer

Abstract

Bladder cancer that occurs on the bladder mucosa is the most common malignant tumor in the urinary system. Exposure to aromatic amine chemicals and cigarette smoking are the two risk factors which causes bladder cancer. The mechanism of complex molecular signaling during its progress is still not understood clearly. High expression of metastasis associated gene 2 (MTA2) in malignant tumors such as ovarian cancer and hepatocellular carcinoma indicates its possible relationship with migration and invasion. However, expression level and biological function of MTA2 in bladder cancer tissues have not been studied. Here, we investigated the biological function, regulation mechanism and clinical application of metastasisrelated genes 2 (MTA2). The expression level of MTA2 in various bladder tumor cells was determined by Western Blot. T24 and EJ cells were selected for in vitro study. T24 cells and EJ cells were transfected with viral vector and SiMTA2, respectively, to induce MTA2 over- or low- expression. MTS colorimetric assay was used to explore the proliferative ability of bladder cancer cells in vitro under MTA2 over- or low-expression. Matrigel invasion assay and Transwell migration assay were used to detect the invasion and migration of cancer cells in vitro under different MTA2 expression conditions. The results of Western Blot assay on bladder cancer cell lines have shown that the MTA2expression level to be significantly lower in T24 cells compared to that of EJ and J82 cells. MTA2 level was significantly higher in MTA2 overexpressed T24 cells than those in the non-transfected and CD511B transfected bladder cancer cells, while the level of MTA2 was much lower in the MTA2-knockdown EJ cells than that in the non-transfected and si-NC transfected. The MTS colorimetric assay significant increase in proliferation of T24 cells with MTA2 overexpression, while the proliferation of EJ cells with MTA2 knockdown was decreased. Results of Transwell migration assay showed that MTA2 overexpression could significantly increase the migration ability of T24 cells, and MTA2 knockdown could significantly reduce the migration ability of EJ cells. Matrigel invasion assay showed that MTA2 overexpression could enhance the invasive ability of T24 cells significantly, while MTA2 knockdown weaken the invasive ability of EJ cells. The expression level of E-cadherin was lower in the T24 cells with MTA2 overexpression than that in the non-transfected group and CD511B transfected group, but the expression level of N-cadherin protein was significantly higher in the T24 cells with MTA2 overexpression compared to the other two groups. The expression level of E-cadherin protein was significantly higher in the EJ cells with MTA2 knockdown than that of the non-transfected group and si-NC transfected group, while the expression level of N-cadherin protein was significantly lower than that in the non-transfected group and si-NC transfected group.