MicroRNA10b suppresses the migration and invasion of chondrosarcoma cells by targeting brainderived neurotrophic factor

Author： Aili Abudunaibi Chen Yong Zhang Hongqi

E-ISSN： 1791-3004|13|1|441-446

ISSN： 1791-2997

Source： Molecular Medicine Reports, Vol.13, Iss.1, 2016-01, pp. : 441-446

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Abstract

MicroRNAs (miRs) can lead to mRNA degradation or inhibit protein translation through directly binding to the 3'untranslational region (UTR) of their target mRNAs. Deregulation of miR10b has been reported to be associated with chondrosarcoma. However, the role of miR10b in chondrosarcoma cell migration and invasion, as well as the underlying mechanisms, has not been investigated. In the present study, it was demonstrated that miR10b was notably downregulated in the JJ012 and SW1353 chondrosarcoma cell lines compared with the TC28a2 normal chondrocyte line. Treatment with DNA demethylating agent 5aza2'deoxycytidine and histone deacetylase inhibitor 4phenylbutyric acid, or transfection with miR10b mimics promoted the expression of miR10b, which further suppressed the migratory and invasive capacities of JJ012 chondrosarcoma cells. Moreover, brainderived neurotrophic factor (BDNF) was identified as a novel target of miR10b, and its protein expression level was negatively regulated by miR10b in JJ012 cells. Furthermore, overexpression of BDNF reversed the inhibitory effect of miR10b upregulation on the migration and invasion of JJ012 cells. In addition, the data suggest that matrix metalloproteinase 1 (MMP1) may be involved in the miR10b/BDNFmediated chondrosarcoma cell migration and invasion in JJ012 cells. In conclusion, these findings suggest that miR10b/BDNF may serve as a potential therapeutic target for chondrosarcoma.