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. 2021 Mar 5;16(3):e0248168. doi: 10.1371/journal.pone.0248168

Fig 5. Schematic summary of a proposed model depicting functional impacts of HOTAIR genetic variations on endometriosis development.

Fig 5

Genetic variations at SNP sites, rs1838169 (C to G) and rs17720428 (T to G), in HOTAIR are frequently detected in patients with endometriosis. Such genetic substitutions alter thermo-stability of mature HOTAIR and stabilize its RNA structure. Through epigenetic silencing by H3K27 tri‐methylation or H3K4-demethylation, higher HOTAIR levels in endometriosis patients can down-regulate its down-stream effectors, such as HOXD10 and HOXA5, leading to increased cell proliferation and migration/invasion.