MIAT and neoplasm: 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.