By targeting PRC2 and mediating histone H3 lysine 27 (H3K27) trimethylation, HOTAIR induces PRC2 occupancy and alters many genes involved in cell-cell signaling and development pathways, leading to tumor metastasis, invasion, and angiogenesis.[54] Its ability to induce breast cancer growth and metastasis was also demonstrated by Ren et al[55] that elevated HOTAIR expression facilitated EMT and tumor metastasis. This evidence concerns the gene HOTAIR and neoplasm.