UCA1 and neoplasm: By associating with EZH2, HEIH represses CDKIs p16 and p21, and thus plays a key role in G0/G1 arrest and promotes tumor progression; UCA1 inhibits CDKI p27, leading to increased expression of CDK2 (a member of CDKs), thus facilitating G1/S transition and accelerating cell cycle progression, whereas HOTAIR decreases p16 and p14 through inhibiting miR-218 expression and increasing Bmi-1 expression and thus contributes to hepatocarcinogenesis [13,17,30].