ArticlePloS one2013
BMPR1B up-regulation via a miRNA binding site variation defines endometriosis susceptibility and CA125 levels.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Ethnic-specific genetic susceptibility loci for endometriosis in Taiwanese-Han population: a genome-wide association study.Journal of human genetics · 2024Article
- TNFα-induced altered miRNA expression links to NF-κB signaling pathway in endometriosis.Research square · 2023Article
- Endometriosis Stem Cells as a Possible Main Target for Carcinogenesis of Endometriosis-Associated Ovarian Cancer (EAOC).Cancers · 2022Review
- A unique 15-bp InDel in the first intron of BMPR1B regulates its expression in Taihu pigs.BMC genomics · 2022Article
- Inflammatory MicroRNAs and the Pathophysiology of Endometriosis and Atherosclerosis: Common Pathways and Future Directions Towards Elucidating the Relationship.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- Genetic impacts on thermostability of onco-lncRNA HOTAIR during the development and progression of endometriosis.PloS one · 2021Article
- Investigating the expressions of miRNA-125b andInternational journal of reproductive biomedicine · 2020Article
- GTF2IRD1 overexpression promotes tumor progression and correlates with less CD8+ T cells infiltration in pancreatic cancer.Bioscience reports · 2020Article
- Malignant Transformation and Associated Biomarkers of Ovarian Endometriosis: A Narrative Review.Advances in therapy · 2020Review
- Plasma miRNAs as biomarkers for endometriosis.Human reproduction (Oxford, England) · 2019Article
- MicroRNAs in endometriosis: biological function and emerging biomarker candidates†.Biology of reproduction · 2019Review
- The TGF-β Family in the Reproductive Tract.Cold Spring Harbor perspectives in biology · 2017Review
- Up-regulation of ribosome biogenesis by MIR196A2 genetic variation promotes endometriosis development and progression.Oncotarget · 2016Article
- Signaling Receptors for TGF-β Family Members.Cold Spring Harbor perspectives in biology · 2016Review
- Review
- Genetic variations of MUC17 are associated with endometriosis development and related infertility.BMC medical genetics · 2015Article
- Cardio-miRNAs and onco-miRNAs: circulating miRNA-based diagnostics for non-cancerous and cancerous diseases.Frontiers in cell and developmental biology · 2014Review
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBone morphogenetic protein receptor I B (BMPR1B) is a transmembrane receptor mediating TGF-β signal transduction. Recent studies indicate a tumor suppressor role for BMPR1B in ovarian cancer. Polymorphism at BMPR1B 3'UTR within the miR-125b binding site alters its binding affinity toward the miRNA, which may result in insufficient post-transcriptional repression.
methodsSingle-nucleotide polymorphisms rs1970801, rs1434536, and rs11097457 near the miR-125b binding site in BMPR1B were genotyped by Taqman assay on 193 endometriosis patients and 202 healthy controls. BMPR1B and CA125 levels in ectopic endometrial tissues were evaluated by quantitative PCR and immunohistochemistry. Luciferase reporter assay was utilized to verify regulatory roles of BMPR1B 3'UTR with allelic variants of rs1434536 in a cell line model. Cell proliferation and migration were recorded, while expression of BMPR1B, CA125, glucocorticoid receptor (GCCR) and IL-1β were measured by quantitative PCR in endometrial cells transfected with wild-type or mutated miR-125b.
resultsThis study found two endometriosis-associated SNPs, rs1434536 (P = 0.010) and rs1970801 (P = 0.0087), located within and next to a miR-125b binding site on BMPR1B. Interestingly, patients with homozygous variant alleles at rs1434536 showed significantly lower serum CA125 levels. Immunohistochemistry staining further confirmed inverse correlation between BMPR1B and CA125 levels in three rs1434536 genotypes. Cell assays demonstrated the variant allele of rs1434536 up-regulating BMPR1B at both mRNA and protein levels, which negatively correlated with CA125 and IL-1β levels. Disruption of the binding between miR-125b and BMPR1B hampered abnormal cell proliferation.
conclusionsSNPs of BMPR1B within and next to the miR-125b binding site manifested strong correlation with endometriosis development in a Taiwanese cohort. Disrupting the binding of miR-125b toward BMPR1B would increase protein expression, diminishing abnormal cell proliferation as well as serum and cellular CA125 levels. Genetic variation at the miR-125b binding site may play functional roles to protect against endometriosis progression.
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