Mechanistically, we reported that miat acted as a ceRNA by sponging miR-22-3p to upregulated the expression of sirt1. Finally, we identified the miat silencing could inhibit HCC tumorigenesis by inducing HCC cellular senescence and activating p53/p21 andp16/pRb signaling pathways, which promote the production of SASP, and that the anticancer function of SASP accelerates the clearance of HCC tumor cells to limit HCC progression. This evidence concerns the gene TP53 and neoplasm.