Schematic representation of a proposed model depicting functional influences of genetic variations in BMPR1B 3′UTR on endometriosis development.

Cherry Yin-Yi Chang (493833), Yi Chen (38576), Ming-Tsung Lai (493834), Hui-Wen Chang (209955), Jack Cheng (493835), Carmen Chan (493836), Chih-Mei Chen (309456), Shan-Chih Lee (493837), Ying-Ju Lin (419103), Lei Wan (290406), Pei-Wen Tsai (227589), Su-Han Yang (493838), Ching Chung (493839), Jim Jinn-Chyuan Sheu (493840), Fuu-Jen Tsai (230856)
2015 · doi:10.1371/journal.pone.0080630.g004 · W6960440568
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-08-06 ⓘ

Genetic variations in the BMPR1B 3'UTR reduce miR-125b binding, increasing BMPR1B and decreasing cell proliferation and migration, thus lowering endometriosis risk.

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⚙ AI-generated deep summary by qwen3.7-flash, 2026-09-04 · read from full text ⓘ

The study proposes a model where genetic variations in the BMPR1B 3′UTR impair miR-125b binding, leading to up-regulation of BMPR1B expression. Elevated BMPR1B levels in endometrial cells suppress cell proliferation and migration by down-regulating IL-1β, which is associated with a reduced risk of developing endometriosis. Additionally, CA125 levels, a biomarker for the disease, were found to be inversely correlated with BMPR1B in these cells. This paper is centrally about endometriosis — specifically investigating how genetic variations in BMPR1B influence susceptibility through miRNA-mediated regulation.

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Abstract

Mature miRNAs including miR-125b are produced by several processing steps where the microprocessor complex (Drosha/DGCR8), exportin 5 and Dicer/TRBP/PACT complex have been known to involve in. The resulting miR-125b forms a RISC complex with Ago and silences BMPR1B gene by binding to the complementary sequence in BMPR1B 3′UTR. Impaired recognition due to genetic variations in the mir-125b seed region reduces suppressive effect of mir-125b, resulting in up-regulation of BMPR1B. The CA125 level, a biomarker for endometriosis and ovarian cancer, was found reversely correlated with BMPR1B in endometrium cells. Elevated BMPR1B levels in endometrium cells have been proven to reduce cell proliferation and migration activity via down-regulation of IL-1β, indicating a lower risk to develop endometriosis.
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BMPR1B Up-Regulation via a miRNA Binding Site Variation Defines Endometriosis Susceptibility and CA125 Levels Figure 4 Schematic representation of a proposed model depicting functional influences of genetic variations in BMPR1B 3′UTR on endometriosis development. Mature miRNAs including miR-125b are produced by several processing steps where the microprocessor complex (Drosha/DGCR8), exportin 5 and Dicer/TRBP/PACT complex have been known to involve in. The resulting miR-125b forms a RISC complex with Ago and silences BMPR1B gene by binding to the complementary sequence in BMPR1B 3′UTR. Impaired recognition due to genetic variations in the mir-125b seed region reduces suppressive effect of mir-125b, resulting in up-regulation of BMPR1B. The CA125 level, a biomarker for endometriosis and ovarian cancer, was found reversely correlated with BMPR1B in endometrium cells. Elevated BMPR1B levels in endometrium cells have been proven to reduce cell proliferation and migration activity via down-regulation of IL-1β, indicating a lower risk to develop endometriosis.

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