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Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Home | Pregnancy Timeline | News Alerts |News Archive Nov 8, 2013

 

The tumor stem cells display increased signaling activity with TGF-beta (TGF-b), a signaling protein already shown to be heavily tied to other craniofacial malformations.

Image Credit: Cell Stem Cell







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Mechanism identified that makes ordinary stem cells create tumors

Epigenetic effects on cell signaling leads healthy stem cells to create benign fibromas in the jaw — which could become harmful.

A new study from the Ostrow School of Dentistry published in Cell Stem Cell illustrates how changes in cell signaling can cause ordinary stem cells in the jaw to start forming benign but potentially harmful tumors. The study was led by Songtao Shi, principal investigator, and professor at the Ostrow School of Dentistry Center for Craniofacial Molecular Biology.


Dr. Songtao Shi says ossifying fibromas, the tumors focused on in the study, are benign but can grow aggressively, causing progressive enlargement of the jaw.


"The only treatment option for ossifying fibromas is surgical, which leads to major loss of vital tissues and challenging post-surgical reconstruction," Shi says. "Quality of life is largely compromised. Thus, there is an urgent need to understand the underlying mechanism by which stem cells may contribute to the pathophysiology of orofacial benign tumors and to develop target-specific treatment."

Shi and his collaborators uncovered a cellular signaling pathway that converts healthy mesenchymal stem cells in the jaw into ossifying fibroma mesenchymal stem cells (OFMSC), lessening their ability to make healthy bone tissue and greatly increasing the rate at which they multiply. The tumor stem cells display increased signaling activity with TGF-beta (TGF-b), a signaling protein already shown to be heavily tied to other craniofacial malformations.

Epigenetic upregulation means switching existing but inactive genes "on."   The TGF-b cell signaling loop appears to increase the formation of ossifying fibroma tumors.


According to Shi, suppressing TGF-b signaling seems to quell the tumor's proliferation rate.


While there is still much more investigation needed, Shi hopes that the findings have shed light on a way to stop the harmful growth of the tumors before risky surgery is needed.

"With an increased understanding of the mechanism of OFMSC, we can induce them to turn into normal jawbone MSC," he says. "But before we can put this into clinical use, more translational research is needed."

Abstract
Abnormal stem cell function makes a known contribution to many malignant tumors, but the role of stem cells in benign tumors is not well understood. Here, we show that ossifying fibroma (OF) contains a stem cell population that resembles mesenchymal stem cells (OFMSCs) and is capable of generating OF-like tumor xenografts. Mechanistically, OFMSCs show enhanced TGF-β signaling that induces aberrant proliferation and deficient osteogenesis via Notch and BMP signaling pathways, respectively. The elevated TGF-β activity is tightly regulated by JHDM1D-mediated epigenetic regulation of thrombospondin-1 (TSP1), forming a JHDM1D/TSP1/TGF-β/SMAD3 autocrine loop. Inhibition of TGF-β signaling in OFMSCs can rescue their abnormal osteogenic differentiation and elevated proliferation rate. Furthermore, chronic activation of TGF-β can convert normal MSCs into OF-like MSCs via establishment of this JHDM1D/TSP1/TGF-β/SMAD3 autocrine loop. These results reveal that epigenetic regulation of TGF-β signaling in MSCs governs the benign tumor phenotype in OF and highlight TGF-β signaling as a candidate therapeutic target.

Cell Stem Cell, Volume 13, Issue 5, 577-589, 7 November 2013
Copyright © 2013 Elsevier Inc. All rights reserved.
10.1016/j.stem.2013.08.010

Authors
Haiyan Qin, Cunye Qu, Takayoshi Yamaza, Ruili Yang, Xia Lin, Xue-Yan Duan, Kentaro Akiyama, Yi Liu, Qunzhou Zhang, Chider Chen, Yibu Chen, Hank Heng Qi, Xin-Hua Feng, Anh D. Le, Songtao Shisend emailSee Affiliations
Highlights
The benign tumor ossifying fibroma contains mesenchymal tumor stem cells (OFMSCs)
Activation of TGF-β signaling contributes to the aberrant function of OFMSCs
TGF-β signaling is upregulated by a JHDM1D/TSP1/TGF-β/SMAD3 autocrine loop
Activation of the JHDM1D/TSP1/TGF-β/SMAD3 loop converts normal MSCs to OF-like MSCs
Summary

The authors of "Ossifying Fibroma Tumor Stem Cells Are Maintained by Epigenetic Regulation of a TSP1/TGF-?/SMAD3 Autocrine Loop" include researchers from USC, the University of Pennsylvania, Baylor College of Medicine, and the University of Iowa. The article first appears in Cell Stem Cell on November 7, 2013. The work was supported by grants from the National Institute of Dental and Craniofacial Research, the National Institutes of Health, Department of Health and Human Services and a grant from the California Institute for Regenerative Medicine.

Original press release: http://www.eurekalert.org/pub_releases/2013-11/uosc-usi110513.php