{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T11:39:29Z","timestamp":1790336369223,"version":"4.1.0"},"reference-count":124,"publisher":"The Company of Biologists","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,1,1]]},"abstract":"<jats:p>The regulation of epithelial proliferation during organ morphogenesis is crucial for normal development, as dysregulation is associated with tumor formation. Non-coding microRNAs (miRNAs), such as miR-200c, are post-transcriptional regulators of genes involved in cancer. However, the role of miR-200c during normal development is unknown. We screened miRNAs expressed in the mouse developing submandibular gland (SMG) and found that miR-200c accumulates in the epithelial end buds. Using both loss- and gain-of-function, we demonstrated that miR-200c reduces epithelial proliferation during SMG morphogenesis. To identify the mechanism, we predicted miR-200c target genes and confirmed their expression during SMG development. We discovered that miR-200c targets the very low density lipoprotein receptor (Vldlr) and its ligand reelin, which unexpectedly regulate FGFR-dependent epithelial proliferation. Thus, we demonstrate that miR-200c influences FGFR-mediated epithelial proliferation during branching morphogenesis via a Vldlr-dependent mechanism. miR-200c and Vldlr may be novel targets for controlling epithelial morphogenesis during glandular repair or regeneration.<\/jats:p>","DOI":"10.1242\/dev.070151","type":"journal-article","created":{"date-parts":[[2011,11,25]],"date-time":"2011-11-25T03:31:52Z","timestamp":1322191912000},"page":"191-202","source":"Crossref","is-referenced-by-count":57,"title":["miR-200c regulates FGFR-dependent epithelial proliferation via Vldlr during submandibular gland branching morphogenesis"],"prefix":"10.1242","volume":"139","author":[{"given":"Ivan T.","family":"Rebustini","sequence":"first","affiliation":[{"name":"Matrix and Morphogenesis Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toru","family":"Hayashi","sequence":"additional","affiliation":[{"name":"Matrix and Morphogenesis Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew D.","family":"Reynolds","sequence":"additional","affiliation":[{"name":"Matrix and Morphogenesis Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melvin L.","family":"Dillard","sequence":"additional","affiliation":[{"name":"Matrix and Morphogenesis Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen M.","family":"Carpenter","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Biobehavioral Science, UCLA School of Medicine, Los Angeles, CA 90095, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew P.","family":"Hoffman","sequence":"additional","affiliation":[{"name":"Matrix and Morphogenesis Section, Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042606183681100_R1","doi-asserted-by":"crossref","first-page":"5060","DOI":"10.1158\/1078-0432.CCR-08-2245","article-title":"miR-200 expression regulates epithelial-to-mesenchymal transition in bladder cancer cells and reverses resistance to epidermal growth factor receptor therapy","volume":"15","author":"Adam","year":"2009","journal-title":"Clin. 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