Background Osteosarcoma (OS) is a common severe illness globally. Lupeol has been reported to participate in the pathophysiologic properties of various cancers, including OS. This study aimed to explore the effects of lupeol on proliferation, invasion, and apoptosis on OS cells and the underlying mechanism. Methods The cell viability of OS cells was determined by 3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. The expression levels of miR-212-3p and high-mobility group AT-hook 2 (HMGA2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in OS cells. The cell apoptosis and invasion were detected by flow cytometry and transwell invasion assays, respectively. The functional target of miR-212-3p was predicted by online software and confirmed by luciferase reporter assay. The protein level of HMGA2 was measured by western blot analysis. Results Lupeol suppressed cell viability and invasion, and promoted apoptosis by upregulating the expression of miR-212-3p in OS cells. Knockdown of miR-212-3p restored the anti-tumor effect of lupeol. Interestingly, miR-212-3p directly targeted HMGA2 and suppressed its expression. Moreover, HMGA2 reversed the inhibited impact on viability and invasion, and the promoted effect on apoptosis induced by upregulation of miR-212-3p. Also, lupeol administration exerts its anti-tumor effect by overexpression of miR-212-3p to suppress the expression of HMGA2 in OS cells. Conclusion Lupeol inhibited OS progression by modulating the miR-212-3p/HMGA2 axis in vitro.
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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