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Recent studies demonstrate the functions of long non-coding RNAs (lncRNAs) in mediating gene expression at the transcriptional or translational level. Our previous study identified a  Sirt1  antisense (AS) lncRNA transcribed from the  Sirt1  AS strand. However, its role and regulatory mechanism is still unknown in myogenesis. Here, functional analyses showed that  Sirt1  AS lncRNA overexpression promoted myoblast proliferation, but inhibited differentiation. Mechanistically,  Sirt1  AS lncRNA was found to activate its sense gene,  Sirt1 . The luciferase assay provided evidences that  Sirt1  AS lncRNA interacted with  Sirt1  3′ UTR and rescued  Sirt1  transcriptional suppression by competing with miR-34a. In addition, RNA stability assay showed that  Sirt1  AS lncRNA prolonged  Sirt1  mRNA half-life from 2 to 10 h. Ribonuclease protection assay further indicated that it fully bound to  Sirt1  mRNA in the myoblast cytoplasm. Moreover,  Sirt1  AS overexpression led to less mouse weight than the control because of less lean mass and greater levels of  Sirt1 , whereas the fat mass and levels of miR-34a were not altered. Based on the findings, a novel regulatory mechanism was found that  Sirt1  AS lncRNA preferably interacted with  Sirt1  mRNA forming RNA duplex to promote  Sirt1  translation by competing with miR-34a, inhibiting muscle formation.

Sirt1 AS lncRNA interacts with its mRNA to inhibit muscle formation by attenuating function of miR-34a