ArticleInternational journal of molecular sciences2012
ACVR1, a therapeutic target of fibrodysplasia ossificans progressiva, is negatively regulated by miR-148a.
Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Molecular, phenotypic aspects and therapeutic horizons of rare genetic bone disorders.BioMed research international · 2014Pooled it
- The role of miRNAs as biomarkers in heterotopic ossification.EFORT open reviews · 2024Review
- Fibrodysplasia ossificans progressiva: Two case reports.Radiology case reports · 2024Article
- The role of miRNA and lncRNA in heterotopic ossification pathogenesis.Stem cell research & therapy · 2022Review
- Promoter methylation-regulated miR-148a-3p inhibits lung adenocarcinoma (LUAD) progression by targeting MAP3K9.Acta pharmacologica Sinica · 2022Article
- Targeting heterotopic ossification by inhibiting activin receptor‑like kinase 2 function (Review).Molecular medicine reports · 2019Review
- Non-coding RNA in endothelial-to-mesenchymal transition.Cardiovascular research · 2019Review
- MicroRNA-148b Targets the TGF-β Pathway to Regulate Angiogenesis and Endothelial-to-Mesenchymal Transition during Skin Wound Healing.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- miR-208a-3p Suppresses Osteoblast Differentiation and Inhibits Bone Formation by Targeting ACVR1.Molecular therapy. Nucleic acids · 2018Article
- The Horizon of a Therapy for Rare Genetic Diseases: A "Druggable" Future for Fibrodysplasia Ossificans Progressiva.International journal of molecular sciences · 2018Review
- The Diverse Mechanisms of miRNAs and lncRNAs in the Maintenance of Liver Cancer Stem Cells.BioMed research international · 2018Review
- Effects of miR-146a on the osteogenesis of adipose-derived mesenchymal stem cells and bone regeneration.Scientific reports · 2017Article
- Copy number variation as a genetic basis for heterotaxy and heterotaxy-spectrum congenital heart defects.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Article
- miR-148a-3p represses proliferation and EMT by establishing regulatory circuits between ERBB3/AKT2/c-myc and DNMT1 in bladder cancer.Cell death & disease · 2016Article
- TGF-β Signaling from Receptors to Smads.Cold Spring Harbor perspectives in biology · 2016Review
- A Survey of Strategies to Modulate the Bone Morphogenetic Protein Signaling Pathway: Current and Future Perspectives.Stem cells international · 2016Review
- Regulatory MiR-148a-ACVR1/BMP circuit defines a cancer stem cell-like aggressive subtype of hepatocellular carcinoma.Hepatology (Baltimore, Md.) · 2015Article
- A genetic variant of miR-148a binding site in the SCRN1 3'-UTR is associated with susceptibility and prognosis of gastric cancer.Scientific reports · 2014Article
- Regulation of ACVR1 and ID2 by cell-secreted exosomes during follicle maturation in the mare.Reproductive biology and endocrinology : RB&E · 2014Article
- MicroRNA-148a is downregulated in gastric cancer, targets MMP7, and indicates tumor invasiveness and poor prognosis.Cancer science · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrodysplasia ossificans progressiva (FOP) is a rare congenital disorder of skeletal malformations and progressive extraskeletal ossification. There is still no effective treatment for FOP. All FOP individuals harbor conserved point mutations in ACVR1 gene that are thought to cause ACVR1 constitutive activation and activate BMP signal pathway. The constitutively active ACVR1 is also found to be able to cause endothelial-to-mesenchymal transition (EndMT) in endothelial cells, which may cause the formation of FOP lesions. MicroRNAs (miRNAs) play an essential role in regulating cell differentiation. Here, we verified that miR-148a directly targeted the 3' UTR of ACVR1 mRNA by reporter gene assays and mutational analysis at the miRNA binding sites, and inhibited ACVR1 both at the protein level and mRNA level. Further, we verified that miR-148a could inhibit the mRNA expression of the Inhibitor of DNA binding (Id) gene family thereby suppressing the BMP signaling pathway. This study suggests miR-148a is an important mediator of ACVR1, thus offering a new potential target for the development of therapeutic agents against FOP.
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Registered trials
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.