NDLI: MicroRNA-34c inversely couples the biological functions of the runt-related transcription factor RUNX2 and the tumor suppressor p53 in osteosarcoma.

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MicroRNA-34c inversely couples the biological functions of the runt-related transcription factor RUNX2 and the tumor suppressor p53 in osteosarcoma.

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MicroRNA-34c inversely couples the biological functions of the runt-related transcription factor RUNX2 and the tumor suppressor p53 in osteosarcoma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dierkes, Christian Cinghu, Senthilkumar Bae, Suk-chul Stein, Janet L. Taipaleenmäki, Hanna Squire, Jeremy A. Ito, Yoshiaki Yaszemski, Michael J. Leong, David T. Hesse, Eric Ling, Ling Cool, Simon M. Galindo, Mario Gupta, Anurag Zustin, Jozef Salto-tellez, Manuel Van Wijnen, Andre J. Lian, Jane B. Zielenska, Maria Zhang, Ying Zambetti, Gerard P. Maran, Avudaiappan Shogren, Kristen Stein, Gary S. Van Der Deen, Margaretha Teplyuk, Nadiya M. Jones, Stephen N.
Description	Author Affiliation: van der Deen M ( Department of Cell Biology and Cancer Center, University of Massachusetts Medical School, Worcester, Massachusetts 01655-0106, USA.)
Abstract	Osteosarcoma (OS) is a primary bone tumor that is most prevalent during adolescence. RUNX2, which stimulates differentiation and suppresses proliferation of osteoblasts, is deregulated in OS. Here, we define pathological roles of RUNX2 in the etiology of OS and mechanisms by which RUNX2 expression is stimulated. RUNX2 is often highly expressed in human OS biopsies and cell lines. Small interference RNA-mediated depletion of RUNX2 inhibits growth of U2OS OS cells. RUNX2 levels are inversely linked to loss of p53 (which predisposes to OS) in distinct OS cell lines and osteoblasts. RUNX2 protein levels decrease upon stabilization of p53 with the MDM2 inhibitor Nutlin-3. Elevated RUNX2 protein expression is post-transcriptionally regulated and directly linked to diminished expression of several validated RUNX2 targeting microRNAs in human OS cells compared with mesenchymal progenitor cells. The p53-dependent miR-34c is the most significantly down-regulated RUNX2 targeting microRNAs in OS. Exogenous supplementation of miR-34c markedly decreases RUNX2 protein levels, whereas 3'-UTR reporter assays establish RUNX2 as a direct target of miR-34c in OS cells. Importantly, Nutlin-3-mediated stabilization of p53 increases expression of miR-34c and decreases RUNX2. Thus, a novel p53-miR-34c-RUNX2 network controls cell growth of osseous cells and is compromised in OS.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	29
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-07-19
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Bone Neoplasms Metabolism Core Binding Factor Alpha 1 Subunit MicroRNAs Osteosarcoma Tumor Suppressor Protein P53 Animals Genetics Pathology Cell Cycle Radiation Effects Cell Line, Tumor Cell Proliferation Cyclin-Dependent Kinase Inhibitor P21 DNA Damage Down-Regulation Gamma Rays Gene Expression Regulation, Neoplastic Mice Protein Stability RNA, Messenger Tumor Suppressor Protein P14ARF Deficiency Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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