Altering their interaction through the HOTAIR/miR-34a-5p axis could suppress Snail expression, thereby increasing E-cadherin levels and repressing EMT.[20] Consistently, similar expression was found in esophageal cancer and PDAC, where HOTAIR acts as a competing endogenous lncRNA (ceRNA) to accelerate tumorigenesis by sponging miRNA.[58,59]. This evidence concerns the gene SNAI1 and esophageal cancer.