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Open Access miR-223 regulates proliferation and apoptosis by targeting insulin-like growth factor 1 receptor (IGF1R) in osteosarcoma cells

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MicroRNAs are widely involved in cancer progression by inhibiting the expression levels of oncogenes or tumor-suppressor genes, and the dysregulation of microRNAs may contribute to tumorigenesis. Here, we use molecular-biology and cell-biology methods to determine the role of miR-223 in osteosarcoma (OS) regulation. The regulating effect of miR-223 on OS is determined by various experimental methods in vivo and in vitro. Exogenous miR-223 reduces the proliferation of HOS and MG-63 cells in vitro. In addition, we show that excessive expression of miR-223 significantly increases apoptosis of OS cells. Moreover, the insulin-like growth factor 1 receptor (IGF-1R) is downgraded after using an miR-223 simulated transfection in HOS and MG-63 cells. After IGF-1R inhibition, the cell activity of the HOS and MG-63 cells is also inhibited. In addition, we demonstrate that miR-223 inhibits OS proliferation and induces apoptosis by targeting a point in IGF-1R 3′ -UTR. In summary, miR-223 inhibits OS proliferation and induces apoptosis by targeting IGF-1R. New therapies with fewer complications based on miRNAs should be studied.

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Document Type: Research Article

Publication date: August 1, 2019

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  • Materials Express is a peer-reviewed multidisciplinary journal reporting emerging researches on materials science, engineering, technology and biology. Cutting-edge researches on the synthesis, characterization, properties, and applications of a very wide range of materials are covered for broad readership; from physical sciences to life sciences. In particular, the journal aims to report advanced materials with interesting electronic, magnetic, optical, mechanical and catalytic properties for industrial applications.
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