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. 2016 Oct 27;7(10):e2436. doi: 10.1038/cddis.2016.325

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Copyright © 2016 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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miR-203 inhibits the osteogenic differentiation of osteoblasts. The hFOB1.19 cells transfected with agomiR-203, antagomiR-203, or their controls were cultured in OM for 3 weeks. (a) Representative images of alizarin red S staining. (b) Quantitative analysis of matrix mineralization. (c) Changes in the miR-203 level during osteogenesis in hFOB1.19 cells were detected by RT-PCR analysis. (d) The expression of the Runx2, β-catenin, p-ERK and ERK proteins during osteogenesis was detected by western blot analysis. (e) The hFOB1.19 cells were transfected with agomiR-203, antagomiR-203 or their controls for 48 h, relative mRNA level of Wnt 3a was detected by real-time PCR. (f) The knockdown efficiency of Runx2 siRNA was confirmed by western blot analysis. (g) Real-time PCR analysis of OCN, ALP and BSP mRNA in hFOB1.19 cells after co-transfecting Runx2 siRNA with agomiR-203, antagomiR-203 or their NCs for 3 days. All of the data are expressed as the means±S.D. from three independent experiments. *P<0.01; NS, not significant