ArticleProceedings of the National Academy of Sciences of the United States of America2013
Loss of the repressor REST in uterine fibroids promotes aberrant G protein-coupled receptor 10 expression and activates mammalian target of rapamycin pathway.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 87 citations in OpenAlex.
- NAV3, a Tumor Suppressor Gene, Is Decreased in Uterine Leiomyoma Tissue and Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2020Trial
- Prolactin-Releasing Hormone Receptor (PRLHR) enhances radiosensitivity and exacerbates DNA damage in glioblastoma post-irradiation by inhibiting Y-box-binding protein-1 (YBX1) nuclear translocation: a novel perspective on precision radiotherapy.Molecular biomedicine · 2026Article
- The molecular role of RE1 silencing transcription factor in uterine diseases: is there potential for targeted therapeutic development?Expert opinion on therapeutic targets · 2025Article
- Molecular dynamics simulations based siRNA design against GPR10 reveals stable RNAi therapeutics for hormone-dependent uterine fibroids.Scientific reports · 2025Article
- Combining a novel ensemble model and multiplex methylation SNaPshot assays for saliva age prediction and cross-platform data analysis.BMC genomics · 2025Article
- Loss of PRICKLE1 leads to subfertility, aberrant extracellular matrix and abnormal myometrial architecture in mice.Reproduction (Cambridge, England) · 2025Article
- Loss of PRICKLE1 leads to abnormal endometrial epithelial architecture, decreased embryo implantation, and reduced fertility in mice.PNAS nexus · 2025Article
- Review
- REST missense mutations reveal disrupted Re1 motif binding and co-repressor interactions in uterine fibroids.Frontiers in bioinformatics · 2025Article
- Establishment of 3D Cultures of Myometrium, Leiomyoma, and Leiomyosarcoma Cells: Advantages and Disadvantages of Two Different Models.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Estrogen receptor alpha mediated repression of PRICKLE1 destabilizes REST and promotes uterine fibroid pathogenesis.bioRxiv : the preprint server for biology · 2024Article
- Functional Analysis of RE1 Silencing Transcription Factor as a Putative Tumor Suppressor in Human Endometrial Cancer.International journal of molecular sciences · 2024Article
- Altered extracellular matrix-related pathways accelerate the transition from normal to prefibroid myometrium in Black women.American journal of obstetrics and gynecology · 2024Article
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
- Loss of the repressor REST affects progesterone receptor function and promotes uterine leiomyoma pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Single-cell sequencing reveals novel cellular heterogeneity in uterine leiomyomas.Human reproduction (Oxford, England) · 2022Article
- Comprehensive Review of Uterine Fibroids: Developmental Origin, Pathogenesis, and Treatment.Endocrine reviews · 2022Review
- Loss of REST in breast cancer promotes tumor progression through estrogen sensitization, MMP24 and CEMIP overexpression.BMC cancer · 2022Article
- PRLHR Immune Genes Associated With Tumor Mutation Burden can be Used as Prognostic Markers in Patients With Gliomas.Frontiers in oncology · 2022Article
- Uterine Fibroids: Hiding in Plain Sight.Physiology (Bethesda, Md.) · 2022Review
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9 authors at 2 institutions in 1 country.
Funding
Abstract
Uterine fibroids (leiomyomas) are the most common tumors of the female reproductive tract, occurring in up to 77% of reproductive-aged women, yet molecular pathogenesis remains poorly understood. A role for atypically activated mammalian target of rapamycin (mTOR) pathway in the pathogenesis of uterine fibroids has been suggested in several studies. We identified that G protein-coupled receptor 10 [GPR10, a putative signaling protein upstream of the phosphoinositide 3-kinase-protein kinase B/AKT-mammalian target of rapamycin (PI3K/AKT-mTOR) pathway] is aberrantly expressed in uterine fibroids. The activation of GPR10 by its cognate ligand, prolactin releasing peptide, promotes PI3K-AKT-mTOR pathways and cell proliferation specifically in cultured primary leiomyoma cells. Additionally, we report that RE1 suppressing transcription factor/neuron-restrictive silencing factor (REST/NRSF), a known tumor suppressor, transcriptionally represses GPR10 in the normal myometrium, and that the loss of REST in fibroids permits GPR10 expression. Importantly, mice overexpressing human GPR10 in the myometrium develop myometrial hyperplasia with excessive extracellular matrix deposition, a hallmark of uterine fibroids. We demonstrate previously unrecognized roles for GPR10 and its upstream regulator REST in the pathogenesis of uterine fibroids. Importantly, we report a unique genetically modified mouse model for a gene that is misexpressed in uterine fibroids.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.