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To investigate the role of MetaLnc9 in the osteogenesis of human bone marrow mesenchymal stem cells (hBMSCs). We used lentiviruses to knockdown or overexpress MetaLnc9 in hBMSCs. qRT-PCR was employed to determine the mRNA levels of osteogenic-related genes in transfected cells. ALP staining and activity assay, ARS staining and quantification were used to identify the degree of osteogenic differentiation. Ectopic bone formation was conducted to examine the osteogenesis of transfected cells in vivo. AKT pathway activator SC-79 and inhibitor LY294002 were used to validate the relationship between MetaLnc9 and AKT signaling pathway. The expression of MetaLnc9 was significantly upregulated in the osteogenic differentiation of hBMSCs. MetaLnc9 knockdown inhibited the osteogenesis of hBMSCs, whereas overexpression of it promoted the osteogenic differentiation both in vitro and in vivo. Taking a deeper insight, we found that MetaLnc9 enhanced the osteogenic differentiation by activating AKT signaling. The inhibitor of AKT signaling LY294002 could reverse the positive effect on osteogenesis brought by MetaLnc9 overexpression, whereas the activator of AKT signaling SC-79 could reverse the negative effect caused by MetaLnc9 knockdown. Our works uncovered a vital role of MetaLnc9 in osteogenesis via regulating the AKT signaling pathway.

MetaLnc9 facilitates osteogenesis of human bone marrow mesenchymal stem cells by activating the AKT pathway