RADIATION PROTECTION ›› 2021, Vol. 41 ›› Issue (6): 550-557.

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The role of miR-200b in radiation-induced thymic lymphoma and its preliminary mechanism

YE Hui1, FENG Zhelan2,3, CHENG Ying3, CAI Jianming2,3, JIANG Jianming1   

  1. 1. Changhai Hospital, Naval Medical University, Shanghai 200433;
    2. School of Public Health and Management, Wenzhou Medical University, Zhejiang Wenzhou 325035;
    3. Faculty of Naval Medicine, Naval Medical University, Shanghai 200433
  • Received:2021-06-02 Online:2021-11-20 Published:2021-12-06

Abstract: In order to explore the role and mechanism of miR-200b in radiation-induced thymic lymphoma, the radiation-induced thymic lymphoma model of BALB/c mice was established by whole body fractionated irradiation. The expression of miR-200b was detected, and the over expression and knockdown miR-200b cell model was constructed to detect the effect of miRNA on cell proliferation and apoptosis. Then the potential targets of miRNA were analyzed by miRNA database TargetScan and verified by dual luciferase reporter system. Finally, the correlation between TBK1 protein and miR-200b expression was analyzed by Spearman method. The results showed that the expression of miR-200b in mice thymic lymphoma was down-regulated by radiation, over expression of miR-200b could significantly inhibit cell proliferation and promote apoptosis, while down-regulation of miR-200b could promote cell proliferation and inhibit apoptosis, and dual luciferase reporting system suggested that miR-200b targeted TBK1 in a 3'UTR-dependent manner. In radiation-induced thymic lymphoma samples, there was a negative correlation between the expression of miR-200b and the level of TBK1 protein, and the over expression of TBK1 could partially reverse the cellular biological effects mediated by miR-200b. The results showed that the expression of miR-200b was down-regulated and the direct target TBK1 was up-regulated in thymic lymphoma induced by radiation, and the over expression of miR-200b could significantly inhibit the proliferation and increase the apoptosis of thymic lymphoma cells. It is suggested that targeted regulation of miR-200b/TBK1 may be a potential new approach to prevent and treat radiation-induced thymic lymphoma.

Key words: radiation carcinogenesis, radiation induced thymic lymphoma (RITL), miR-200b, TBK1, tumor therapy

CLC Number: 

  • R730