Fig. 4
From: The emerging role of the long non-coding RNA HOTAIR in breast cancer development and treatment
Effect of HOTAIR on epithelial-mesenchymal transition. HOTAIR could promote epithelial-mesenchymal transition (EMT) through at least three pathways. lincRNA HOTAIR activity could indirectly inhibit miR-7. This leads to overexpression of SETDB1, STAT3, c-Myc, twist and miR-9, while E-cadherin is down-regulated. HOTAIR activity could also promote prometastatic activity of cancer cells by regulating VEGF, MMP-9, β-catenin and Vimentin. Moreover, lincRNA HOTAIR could coordinate in tripartite SNAIl/HOTAIR/EZH2 complex. This complex involves in general chromatin modification to inhibit expression of the genes involved in epithelial formation (e.g. HNF4α, HNF1α and E-cadherin)