The Role Of Mir - 203 In Glioma Cells And Its Mechanism Preliminarily

Background and purposeglioma is the most common intracranial malignant tumor, the incidence rate, cure rate of which is low, and is seriously harm to human health. Therefore, to clarify its pathogenesis, and to find new biomarkers and therapeutic targets to improve the therapeutic effect has become a major issue to be solved. This project makes models of A172cells of low degree of malignancy and U87cells of higher degree of malignancy to understand the effect and mechanism of miR-203in the proliferation, migration invasion and chemosensitivity of glioma cell.Methods(1) detect the expression of miR-203in glioma cells, A172and U87by real-time quantitative PCR;(2) build expression vector pSilencer2.1-U6-miR-203of miR-203, transfect miR-203expression vector and miR-203inhibitor into U87and A172cells through liposome, observe the effect on the migration and invasion by scratch test and the Transwell experiment,and observe the effect on proliferation and sensitivity of the Nebo glucoside (VM-26)of the miR-203cell though MTS experiment;(3) bioinformation analyse that the possible target genes of miR-203is E2F3, by Western blot detect the expression of E2F3in all cells.(4) after the synthesis of E2F3antisense oligonucleotides, transfect U87cells though liposome,Western blot analyse the expression of E2F3protein, scratch test and Transwell test observe the effect of interference of E2F3on migration and invasion,the MTS test observe cell proliferation and the sensitivity of the Nebo glucoside (VM-26)after the interference of E2F3.Results (1) compared to A172cells, miR-203expression in U87cells down to8.23±0.390times;(2)miR-203can significantly inhibit the proliferation,migration and invasion of U87cell, increased VM-26chemotherapysensitivity, inhibition of miR-203increases A172cell proliferation and migration and invasion, and reduce the chemosensitivity of VM-26;(3) the3’UTR of E2F3are conserved in the species of miR-203sites of action.miR-203significantly inhibit luciferase activity mediated by the sites, while miR-203and E2F3expression was negatively correlated;(4) lowering the expression of E2F3significantly inhibit the proliferation,migration and invasion of U87cells, increase VM-26sensitivity.Conclusion(1) miR-203can inhibit the proliferation, migration and invasion of glioma cell, increase sensitivity to chemotherapeutic drugs;(2) miR-203directly target at regulation of E2F3protein expression.