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Department of Molecular, Cell and Cancer Biology

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Cell Biology | Developmental Biology | Genetics and Genomics | Molecular Biology | Nucleic Acids, Nucleotides, and Nucleosides


miR-23a, a member of the miR-23a/24-2/27a cluster, has been demonstrated to play pivotal roles in many cellular activities. However, the mechanisms of how bta-miR-23a controls the myogenic differentiation (MD) of PDGFRalpha(-) bovine progenitor cells (bPCs) remain poorly understood. In the present work, bta-miR-23a expression was increased during the MD of (PDGFRalpha-) bPCs. Moreover, bta-miR-23a overexpression significantly promoted the MD of (PDGFRalpha-) bPCs. Luciferase reporter assays showed that the 3'-UTR region of MDFIC (MyoD family inhibitor domain containing) could be a promising target of bta-miR-23a, which resulted in its post-transcriptional down-regulation. Additionally, the knockdown of MDFIC by siRNA facilitated the MD of (PDGFRalpha-) bPCs, while the overexpression of MDFIC inhibited the activating effect of bta-miR-23a during MD. Of note, MDFIC might function through the interaction between MyoG transcription factor and MEF2C promoter. This study reveals that bta-miR-23a can promote the MD of (PDGFRalpha-) bPCs through post-transcriptional downregulation of MDFIC.


MDFIC, bta-miR-23a, fetal muscle development

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Hu X, Xing Y, Ren L, Wang Y, Li Q, Yang Q, Du M, Xu L, Willems L, Li J, Zhang L. bta-miR-23a Regulates the Myogenic Differentiation of Fetal Bovine Skeletal Muscle-Derived Progenitor Cells by Targeting MDFIC Gene. Genes (Basel). 2020 Oct 20;11(10):1232. doi: 10.3390/genes11101232. PMID: 33092227; PMCID: PMC7588927. Link to article on publisher's site

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Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.