Our study revealed that AGAP2-AS1 played a part in promoting PC by interacting with EZH2 and catalyzing H3K27me3 in the ANKRD1 and ANGPTL4 promoter regions in the nucleus, thereby inactivating the tumor suppressors ANKRD1 and ANGPTL4. Abnormal overexpression of EZH2 has been found in various tumor types35–37. This evidence concerns the gene ANGPTL4 and neoplasm.