Upstream mechanism studies have shown that exposure to YY1 in high glucose levels promotes the expression of LINC00842 in tumor cells.[44] YY1 binds to the DICER1-AS1 promoter to promote its transcription, and the up-regulated DICER1-AS1 acts as a sponge for miR-5586-5p and inhibits the expression of glycolysis genes, including LDHA, HK2, PGK1 and SLC2A1.[45] LINC01133 regulates a variety of malignancies, including cancers of the digestive system, female reproductive system, respiratory system and urinary system.[46] LINC01133 can recruit YY1 on its promoter. This evidence concerns the gene LINC01133 and neoplasm.