The role of miR-92a and BCLIIb in radiation induced thymic lymphoma in BALB/c mice

Objective To investigate the expression of miR-92a and BCLllb gene in radiation- induced thymic lymphoma in BALB/e mice, and the regulation of BCL1 l b by miR-92a. Methods BALB/c mice were irradiated with 1.75 Gy gamma rays with a dose rate of 0. 382 Gy/min, 4 weeks in a row and once per week. 6 months after radiation, the incidence of the thymic lymphoma induced by ionizing radiation was checked and the mice were sacrificed. The thymuses of 6 typical mice with thymic lymphoma in the irradiated group and 6 mice in control group were taken for further detection. Real-time PCR were used to detect miR- 92a expression. Western blot and FACS were employed to measure protein expression of BCLllb. The miR- 92a sequence was inserted into pcDNA-DEST-47 plasmid to construct the eukaryotic expression vector （pcDNA-DEST-miR-92a） and to construct the BCL1 lb gene 3＇UTR luciferase reporter plasmid （psiCHECK 2-BCLllb） at the same time. They were used to transfect EL-4 cells together for analysis of the regulation of miR-92a on the expression of BCLIlb. Results The incidence of the thymic lymphoma induced by ionizing radiation was 58.51%. It was found that expression of the tumor suppressor gene BCLllb was down- regulated and expression of miR-92a was up-regulated in radiation induced thymic lymphoma tissue samples. There was an inverse correlation between BCL1 l b protein and miR-92a expression level among different tissue samples （r = - 0. 827, P 〈 0.05）. The expression of luciferase in the group transfected with pcDNA-DEST- miR-92a and psiCHECK 2-BCLllb plasmids was significantly lower than that in the group transfected with empty plasmid and BCLllb gene （t =3.42,P 〈0.05）. Conclusions miR-92a maybe participate in radiation-induced carcinogenesis and regulate the expression of BCL11 b gene. Key words: Ionizing radiation ;  Thymic lymphoma ;  BCL11 b ;  miR-92a