ArticlePLoS genetics2015
Fibroblast Growth Factor 9 Regulation by MicroRNAs Controls Lung Development and Links DICER1 Loss to the Pathogenesis of Pleuropulmonary Blastoma.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- Spatial single cell transcriptomic analysis informs tumor developmental hierarchy of DICER1 syndrome related sarcoma.Nature communications · 2026Article
- Mapping the Natural History of Benign DICER1-Related Lesions and Identifying Predictors of Malignancy.Fortune journal of health sciences · 2026Article
- Umbilical cord blood exosomes from very preterm infants with bronchopulmonary dysplasia aggravate lung injury in mice.Scientific reports · 2023Article
- XRN2 suppresses aberrant entry of tRNA trailers into argonaute in humans and Arabidopsis.PLoS genetics · 2023Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Overexpression of miR-328-5p influences cell growth and migration to promote NSCLC progression by targeting LOXL4.Annals of translational medicine · 2022Article
- The FGFR4 Homolog KIN-9 Regulates Lifespan and Stress Responses inFrontiers in aging · 2022Article
- ETV4 and ETV5 drive synovial sarcoma through cell cycle and DUX4 embryonic pathway control.The Journal of clinical investigation · 2021Article
- Analysis of miRNA Profiles and the Regulatory Network in Congenital Pulmonary Airway Malformations.Frontiers in pediatrics · 2021Article
- Deletion ofDisease models & mechanisms · 2020Article
- miR-187-3p increases gemcitabine sensitivity in breast cancer cells by targeting FGF9 expression.Experimental and therapeutic medicine · 2020Article
- FGF9 and FGF10 activate distinct signaling pathways to direct lung epithelial specification and branching.Science signaling · 2020Article
- NCAM1/FGF module serves as a putative pleuropulmonary blastoma therapeutic target.Oncogenesis · 2019Article
- BiallelicCancer research · 2017Article
- MicroRNA in late lung development and bronchopulmonary dysplasia: the need to demonstrate causality.Molecular and cellular pediatrics · 2016Review
- A network-biology perspective of microRNA function and dysfunction in cancer.Nature reviews. Genetics · 2016Review
- The anti-apoptotic and prognostic value of fibroblast growth factor 9 in gastric cancer.Oncotarget · 2016Article
- Microarray Analyses Reveal Marked Differences in Growth Factor and Receptor Expression Between 8-Cell Human Embryos and Pluripotent Stem Cells.Stem cells and development · 2016Article
- Pleuropulmonary Blastoma: Evolution of an Entity as an Entry into a Familial Tumor Predisposition Syndrome.Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology SocietyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Pleuropulmonary Blastoma (PPB) is the primary neoplastic manifestation of a pediatric cancer predisposition syndrome that is associated with several diseases including cystic nephroma, Wilms tumor, neuroblastoma, rhabdomyosarcoma, medulloblastoma, and ovarian Sertoli-Leydig cell tumor. The primary pathology of PPB, epithelial cysts with stromal hyperplasia and risk for progression to a complex primitive sarcoma, is associated with familial heterozygosity and lesion-associated epithelial loss-of-heterozygosity of DICER1. It has been hypothesized that loss of heterozygosity of DICER1 in lung epithelium is a non-cell autonomous etiology of PPB and a critical pathway that regulates lung development; however, there are no known direct targets of epithelial microRNAs (miRNAs) in the lung. Fibroblast Growth Factor 9 (FGF9) is expressed in the mesothelium and epithelium during lung development and primarily functions to regulate lung mesenchyme; however, there are no known mechanisms that regulate FGF9 expression during lung development. Using mouse genetics and molecular phenotyping of human PPB tissue, we show that FGF9 is overexpressed in lung epithelium in the initial multicystic stage of Type I PPB and that in mice lacking epithelial Dicer1, or induced to overexpress epithelial Fgf9, increased Fgf9 expression results in pulmonary mesenchymal hyperplasia and a multicystic architecture that is histologically and molecularly indistinguishable from Type I PPB. We further show that miR-140 is expressed in lung epithelium, regulates epithelial Fgf9 expression, and regulates pseudoglandular stages of lung development. These studies identify an essential miRNA-FGF9 pathway for lung development and a non-cell autonomous signaling mechanism that contributes to the mesenchymal hyperplasia that is characteristic of Type I PPB.
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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.