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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/112549

    Title: CCN3 Facilitates Runx2 and Osterix Expression by Inhibiting miR-608 through PI3K/Akt Signaling in Osteoblasts
    Authors: 陳?均;Liu, Ju-Fang;Liu, Ju-Fang;Fong, Yi-Chin;Fong, Yi-Chin;黃元勵;HUANG;YUAN-LI;Ch, Chia-Chia;Chao, Chia-Chia;湯智昕;Chih-Hsin;Tang
    Contributors: 生物科技學系
    Date: 2019-07
    Issue Date: 2019-11-15 11:32:25 (UTC+8)
    Abstract: CCN3, otherwise known as the nephroblastoma overexpressed (NOV) protein, is a cysteine-rich protein that belongs to the CCN family and regulates several cellular functions. Osteoblasts are major bone-forming cells that undergo proliferation, mineralization, renewal, and repair during the bone formation process. We have previously reported that CCN3 increases bone morphogenetic protein 4 (BMP-4) production and bone mineralization in osteoblasts, although the role of CCN3 remains unclear with regard to osteogenic transcription factors (runt-related transcription factor 2 (Runx2) and osterix). Here, we used alizarin red-S and alkaline phosphatase staining to show that CCN3 enhances osteoblast differentiation. Stimulation of osteoblasts with CCN3 increases expression of osteogenic factors such as BMPs, Runx2, and osterix. Moreover, we found that the inhibition of miR-608 expression is involved in the effects of CCN3 and that incubation of osteoblasts with CCN3 promotes focal adhesion kinase (FAK) and Akt phosphorylation. Our results indicate that CCN3 promotes the expression of Runx2 and osterix in osteoblasts by inhibiting miR-608 expression via the FAK and Akt signaling pathways.
    Appears in Collections:[生物科技學系] 期刊論文

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