LncRNA MALAT1 promotes osteogenic differentiation through the miR‐217/AKT3 axis: a possible strategy to alleviate osteoporosis

马拉特1 下调和上调 基因敲除 碱性磷酸酶 化学 免疫印迹 癌症研究 细胞生物学 分子生物学
作者
Chenyang Song,Yu Guo,Fenyong Chen,Wenge Liu
出处
期刊:Journal of Gene Medicine [Wiley]
标识
DOI:10.1002/jgm.3409
摘要

Background Accumulating evidence demonstrates that long non-coding RNAs (lncRNAs) are associated with the development of osteoporosis. This study aimed to investigate the effect of MALAT1 on osteogenic differentiation in osteoporosis. Methods The MALAT1 levels were detected by Real-time Polymerase Chain Reaction (RT-qPCR). Moreover, the levels of osteogenic differentiation-related factors (Bmp4, Col1a1, and Spp1) were measured by RT-qPCR and western blot. Alkaline phosphatase (ALP) activity was detected using ALP staining assay. Results The MALAT1 levels were downregulated in hindlimb unloading (HU) mice and simulated microgravity (MG) treated MC3T3-E1 cells. Moreover, MG treatment induced the downregulation of the expression of ALP, BMP4, Col1a1 and Spp1, while overexpression of MALAT1 abolished the downregulation. MG also inhibited ALP activity, while MALAT1 reversed the effect. Furthermore, miR-217 was identified as a target of MALAT1, and AKT3 was verified as a target of miR-217. Overexpression of miR-217 rescued the promotion of osteogenic differentiation induced by MALAT1 in MG treated cells. Knockdown of AKT3 abolished the facilitation of osteogenic differentiation induced by downregulation of miR-217. Conclusion MALAT1 promotes osteogenic differentiation through regulating miR-217/AKT3 axis, suggesting that MALAT1 is a potential target to alleviate osteoporosis.

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