{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T19:21:49Z","timestamp":1788808909485,"version":"build-2803163510"},"reference-count":81,"publisher":"Portland Press Ltd.","issue":"10","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,11,1]]},"abstract":"<jats:p>Bone is increasingly viewed as an endocrine organ with key biological functions. The skeleton produces hormones and cytokines, such as FGF23 and osteocalcin, which regulate an extensive list of homoeostatic functions. Some of these functions include glucose metabolism, male fertility, blood cell production and calcium\/phosphate metabolism. Many of the genes regulating these functions are specific to bone cells. Some of these genes can be wrongly expressed by other malfunctioning cells, driving the generation of disease. The miRNAs are a class of non-coding RNA molecules that are powerful regulators of gene expression by suppressing and fine-tuning target mRNAs. Expression of one such miRNA, miR-140, is ubiquitous in chondrocyte cells during embryonic bone development. Activity in cells found in the adult breast, colon and lung tissue can silence genes required for tumour suppression. The realization that the same miRNA can be both normal and detrimental, depending on the cell, tissue and time point, provides a captivating twist to the study of whole-organism functional genomics. With the recent interest in miRNAs in bone biology and RNA-based therapeutics on the horizon, we present a review on the role of miR-140 in the molecular events that govern bone formation in the embryo. Cellular pathways involving miR-140 may be reactivated or inhibited when treating skeletal injury or disorder in adulthood. These pathways may also provide a novel model system when studying cancer biology of other cells and tissues.<\/jats:p>","DOI":"10.1042\/cs20150230","type":"journal-article","created":{"date-parts":[[2015,8,29]],"date-time":"2015-08-29T02:04:19Z","timestamp":1440813859000},"page":"863-873","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Role of <i>miR-140<\/i> in embryonic bone development and cancer"],"prefix":"10.1042","volume":"129","author":[{"given":"Darrell","family":"Green","sequence":"first","affiliation":[{"name":"Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich, Norfolk NR4 7TJ, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamas","family":"Dalmay","sequence":"additional","affiliation":[{"name":"School of Biological Sciences, University of East Anglia, Norwich Research Park, Norwich, Norfolk NR4 7TJ, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William\u00a0D.","family":"Fraser","sequence":"additional","affiliation":[{"name":"Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich, Norfolk NR4 7TJ, U.K."},{"name":"Department of Endocrinology, Norfolk and Norwich University Hospital, Norwich Research Park, Norwich, Norfolk NR4 7TJ, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2015,8,28]]},"reference":[{"key":"2021113010371246500_B1","doi-asserted-by":"publisher","first-page":"393","DOI":"10.3109\/17453674.2011.588861","article-title":"Where did bone come from?","volume":"82","author":"Wagner","year":"2011","journal-title":"Acta Orthop."},{"key":"2021113010371246500_B2","doi-asserted-by":"publisher","first-page":"43","DOI":"10.1016\/S0959-437X(03)00007-8","article-title":"RUNX transcription factors as key targets of TGF-beta superfamily signaling","volume":"13","author":"Ito","year":"2003","journal-title":"Curr. 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