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    • It is the first time to

    2018-10-26

    It is the first time to report the involvement of miRNA-30c in enhancing sphere formation and neural differentiation. The relationships of miRNA-30c and osteodifferentiation and adipocyte differentiation have been discussed previously (Gao et al., 2011; Karbiener et al., 2011; Vimalraj and Selvamurugan, 2014). We will further analyze if miR-30c-overexpression affects the expression of miR124a or miR9 (miRNAs known to play a key role in neurogenesis) and miRNA-199a-5p and miRNA-145 (oligodendrocyte development). The protein expression level of GFAP was inhibited in miRNA-30c-overexpressing sphere order RGFP966 after IBMX induction compared with the control group. By elevating the level of intracellular cAMP, IBMX is known to induce the astrocytic differentiation of C6 glioma cells by activating the JAK-STAT pathway (Bonni et al., 1997; Takanaga et al., 2004). In the present experiments, the protein level of p-STAT3 was also decreased in miRNA-30c-overexpressing IBMX-induced C6 sphere cells. In Moorthi\'s report, the JAK-STAT3 pathway was affected by miRNA-30c, suggesting that target genes might exist in this pathway (Moorthi et al., 2013). Here, pik3cd, socs3, and jak1, the putative target genes for miRNA-30c in the JAK-STAT3 pathway, were examined by real-time PCR. The decreased mRNA levels of pik3cd and socs3 might explain the inhibited p-STAT3 expression in miRNA-30c-overexpressing IBMX-induced C6 cells (Fig. 7). Qin et al. reported that the activation of STAT3 leads to SOCS3 expression in astrocyte cultures (Qin et al., 2008). In Baker\'s study, oncostatin M stimulated cultured astrocytes and induced SOCS3 expression; the expression decreased with time and p-STAT3 showed similar expression pattern as SOCS3 (Baker et al., 2008). When SOCS3 was expressed in neural stem cells, the number of MAP2-positive cells increased and the number of GFAP-positive cells decreased, indicating that overexpression of SOCS3 can regulate neurogenesis and astrogenesis in neural stem cells (Cao et al., 2006). These results might help us to identify the miRNA-30c-regulated target genes acting during neural differentiation.
    Conclusions
    List of abbreviations
    Authors\' contributions
    Acknowledgments This work was supported by grants to C.-L. Chien (MOST102-2321-B-002-032 and NSC-98-3111-B-002-004) from the Ministry of Science and Technology, Taiwan. The facilities provided by grants from the Ministry of Education, Taiwan to the Center of Genomic Medicine in National Taiwan University are also acknowledged.
    Introduction Bone marrow (BM) is the site of hematopoiesis and is composed of hematopoietic cells (HCs) and their niche, which includes BM stromal cells (BMSCs), osteoblastic cells, osteoclasts, skeletal stem cells, endothelial cells, endosteal monocytes/macrophages, and sympathetic nervous system neurons (Sacchetti et al., 2007; Smith and Calvi, 2013). The hematopoietic niche is the physical locale of the microenvironment that regulates self-renewal, proliferation and differentiation of HCs and protects HCs from oncogenic, physical and chemical damage (Oh and Humphries, 2012). BMSCs have been reported to control hematopoiesis through the production of cytokines that are active in effective hematopoiesis and to support T cell and B cell survival by preventing apoptosis (English, 2013; Majumdar et al., 2000). Myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) are HC neoplasias, and their leukemogenic process is initiated by the accumulation of inherited and randomly acquired genetic aberrations. Cytogenetic abnormalities and gene mutations in MDS and AML are well-known and have been recognized in the World Health Organization classification (Swerdlow et al., 2008) and revised international prognostic scoring system for MDS (Greenberg et al., 2012). In addition, many hematologic neoplasias also acquire epigenetic changes, which may have a profound effect at the level of gene expression (Bonifer and Bowen, 2010; Jelinek et al., 2011). For example, the inactivation of tumor suppressor genes by promoter hypermethylation contributes to the initiation and progression of MDS and AML (Bies et al., 2010; Cechova et al., 2012).