Figure 3.

HOTAIR is the target of several sets of molecules. Anti-cancer agents (metformin, imatinib, and lapatinib) and bioactive molecules (calycosin, genistein, delphinidin, and delphinidin-3-glucoside) target and inhibit HOTAIR through multiple signal pathways. Consequently, HOTAIR ablation suppresses tumor progression by reversing epidermal-mesenchymal transition (EMT) and decreasing migration, invasion and viability, along with promoting apoptosis. HOTAIR-EZH2 inhibitors PNA, AQB, and ADQ can disrupt the interactions, thus blocking the binding of the PRC2 complex to HOTAIR, which eventually attenuate cancer development.