Study On The Molecular Mechanism Of SNORD126 In Promoting Adipogenesis In Cells And Rats By Activating The PI3K–AKT Pathway

In numerous progresses of histogenesis,small nucleolar RNA(sno RNA)plays crucial roles.But,there are no reports about the function of sno RNA in adipogenesis at present.SNORD126 is a C/D box sno RNA.In our previous study,it has been identified that SNORD126 promoted hepatocellular carcinoma cell(HCC)proliferation by activating the phosphoinositide 3-kinase-protein kinase B(PI3K-AKT)pathway through increasing fibroblast growth factor receptor 2(FGFR2)expression.In the present study,we found that SNORD126 was down-regulated in the obesity-related tissues from high fat diet fed rats.Moreover,overexpression of SNORD126 in 3T3-L1 cells stimulated adipocytes differentiation.In addition,SNORD126 strongly upregulated the expression of CCAAT/enhancer-binding protein ?(C/EBP?),fatty acid?binding protein 4(FABP4),peroxisome proliferative-activated receptor ?(PPAR?),and the phosphorylation of AKT and P70S6 K.Overexpression of SNORD126 in human adipose-derived stem cells(h ADSCs)stimulated adipogenesis and increased phosphorylation of AKT and P70S6 K.Moreover,SNORD126 accelerated the messenger RNA and protein levels of cyclin D1 and cyclindependent kinase 2(CDK2),which promoted the progression of mitotic clonal expansion(MCE)during the early stage of 3T3?L1 cell differentiation.We further found that SNORD126 promoted the growth of the inguinal fat pad and increased phosphorylation of AKT and P70S6 K in rats.In summary,our results suggested that SNORD126 accelerated MCE and adipocyte differentiation through increasing phosphorylation of AKT and P70S6 K both in vitro and in vivo.