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Type: Journal article
Title: HOPX regulates bone marrow-derived mesenchymal stromal cell fate determination via suppression of adipogenic gene pathways
Author: Hng, C.H.
Camp, E.
Anderson, P.
Breen, J.
Zannettino, A.
Gronthos, S.
Citation: Scientific Reports, 2020; 10(1):1-14
Publisher: Nature Publishing Group
Issue Date: 2020
ISSN: 2045-2322
Statement of
Chee Ho Hng, Esther Camp, Peter Anderson, James Breen, Andrew Zannettino and Stan Gronthos
Abstract: Previous studies of global binding patterns identified the epigenetic factor, EZH2, as a regulator of the homeodomain-only protein homeobox (HOPX) gene expression during bone marrow stromal cell (BMSC) differentiation, suggesting a potential role for HOPX in regulating BMSC lineage specification. In the present study, we confirmed that EZH2 direct binds to the HOPX promoter region, during normal growth and osteogenic differentiation but not under adipogenic inductive conditions. HOPX gene knockdown and overexpression studies demonstrated that HOPX is a promoter of BMSC proliferation and an inhibitor of adipogenesis. However, functional studies failed to observe any affect by HOPX on BMSC osteogenic differentiation. RNA-seq analysis of HOPX overexpressing BMSC during adipogenesis, found HOPX function to be acting through suppression of adipogenic pathways associated genes such as ADIPOQ, FABP4, PLIN1 and PLIN4. These findings suggest that HOPX gene target pathways are critical factors in the regulation of fat metabolism.
Keywords: Cells, Cultured
Mesenchymal Stem Cells
Homeodomain Proteins
Tumor Suppressor Proteins
Cell Differentiation
Cell Proliferation
Young Adult
Enhancer of Zeste Homolog 2 Protein
Description: Published: 09 July 2020
Rights: © The Author(s) 2020. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit
DOI: 10.1038/s41598-020-68261-2
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