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
🔓 Open OA copy Full text JSON View on OpenAlex View at publisher
⚙ AI-generated deep summary by gpt-5.6-luna, 2026-08-11 · read from full text ⓘ

The paper proposes how HOTAIR genetic variation may contribute to endometriosis development and progression, focusing on the SNPs rs1838169 (C>G) and rs17720428 (T>G), which are frequently detected in affected patients. These substitutions are reported to increase the thermostability of mature HOTAIR and stabilize its RNA structure; elevated HOTAIR may then epigenetically silence downstream effectors such as HOXD10 and HOXA5 through H3K27 trimethylation or H3K4 demethylation, promoting cellular proliferation, migration, and invasion. The proposed model describes a mechanistic framework rather than establishing that every step is causally responsible for disease. This paper is centrally about endometriosis — the proposed effects of HOTAIR variants on epigenetic regulation and lesion-associated cellular behavior.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

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.
Full text 746 characters · extracted from oa-doi-fallback · click to expand
Genetic impacts on thermostability of onco-lncRNA HOTAIR during the development and progression of endometriosis Fig 5 Schematic summary of a proposed model depicting functional impacts of HOTAIR genetic variations on endometriosis development. 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.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosis

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.

Source provenance

openalex
last seen: 2026-05-11T08:48:50.894309+00:00
License: CC0 · commercial use OK