Downregulation of miR-10b promotes osteoblast differentiation through targeting Bcl6

MicroRNAs (miRNAs or miRs) have been shown to play a critical role in osteoblast differentiation. miR-10b has been found to be downregulated during osteoblast differentiation; however, its precise effect on osteoblast differentiation remains unknown. In this study, we aimed to investigate the potent...

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Veröffentlicht in:International journal of molecular medicine 2017-06, Vol.39 (6), p.1605-1612
Hauptverfasser: Yang, Jizhou, Wang, Shaojie, Wang, Fengxian, Mu, Xiaohong, Qu, Yi, Zhao, Ziyi, Yu, Xing
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Sprache:eng
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Zusammenfassung:MicroRNAs (miRNAs or miRs) have been shown to play a critical role in osteoblast differentiation. miR-10b has been found to be downregulated during osteoblast differentiation; however, its precise effect on osteoblast differentiation remains unknown. In this study, we aimed to investigate the potential role of miR-10b and the potential underlying mechanism in regulating osteoblast differentiation. We found that miR-10b was downregulated during osteoblast differentiation. Overexpression of miR-10b inhibited osteoblast differentiation, whereas the suppression of miR-10b promoted osteoblast differentiation. Bioinformatics analysis and the dual-luciferase reporter assay demonstrated that miR-10b could target the 3'-untranslated regions of B cell lymphoma 6 (Bcl6) which is an important regulator of osteoblast differentiation. Real‑time quantitative polymerase chain reaction and western blot analysis showed that miR-10b directly regulated Bcl6 expression. Further experiments showed that the overexpression of miR-10b increased the expression of signal transducer and activator of transcription 1 (STAT1) and blocked Runt-related transcription factor 2 (Runx2) nuclear translocation, whereas miR-10b suppression showed an opposite effect. Moreover, the miR-10b suppression-induced effects were partially reversed by Bcl6 knockdown. Taken together, our study suggests that miR-10b contributes to osteoblast differentiation through targeting Bcl6, providing a novel insight into understanding the molecular mechanism underlying osteoblast differentiation and suggesting a potential target for inhibiting bone loss.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2017.2955