To investigate the role of miR-203 in radiation-induced thymic lymphoma (RITL).
MethodsA 60Co irradiator was used for total-body irradiation. MicroRNAs(miRNAs) level was assayed by qRT-PCR. Cell proliferation was assayed by MTT assay. Cell apoptosis was examined by fluorescence activated cell sorter(FACS). Dual luciferase reporter assay system was used to detect the 3′UTR reporter.
ResultsMiR-203 was down-regulated in RITL tissues. Overexpression of miR-203 strongly inhibited the proliferation of both NIH3T3 cells and EL4 cells and vice versa. MiR-203 inhibited cells proliferation and induced apoptosis via TANK-binding kinase (TBK1), SLUG(SNAI2) and Cyclin D1(CCND1).
ConclusionsRadiation down-regulated the level of miR-203 in thymic, which promoted radiation-induced thymic lymphoma by targeting TBK1, SNAI2 and CCND1.