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

Cherry Yin-Yi Chang (7224650), Chung-Chen Tseng (10262915), Ming-Tsung Lai (493834), An-Jen Chiang (688755), Lun-Chien Lo (10262918), Chih-Mei Chen (309456), Man-Ju Yen (10262921), Li Sun (4624), Li Yang (6520), Tritium Hwang (10262924), Fuu-Jen Tsai (230856), Jim Jinn-Chyuan Sheu (7326185)
2021 · doi:10.1371/journal.pone.0248168.g005 · W6942090223
other OA: green CC0
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Abstract

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.

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endometriosis

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