Literature DB >> 22959078

TGF-β family signaling in stem cells.

Masayo Sakaki-Yumoto1, Yoko Katsuno, Rik Derynck.   

Abstract

BACKGROUND: The diversity of cell types and tissue types that originate throughout development derives from the differentiation potential of embryonic stem cells and somatic stem cells. While the former are pluripotent, and thus can give rise to a full differentiation spectrum, the latter have limited differentiation potential but drive tissue remodeling. Additionally cancer tissues also have a small population of self-renewing cells with stem cell properties. These cancer stem cells may arise through dedifferentiation from non-stem cells in cancer tissues, illustrating their plasticity, and may greatly contribute to the resistance of cancers to chemotherapies. SCOPE OF REVIEW: The capacity of the different types of stem cells for self-renewal, the establishment and maintenance of their differentiation potential, and the selection of differentiation programs are greatly defined by the interplay of signaling molecules provided by both the stem cells themselves, and their microenvironment, the niche. Here we discuss common and divergent roles of TGF-β family signaling in the regulation of embryonic, reprogrammed pluripotent, somatic, and cancer stem cells. MAJOR
CONCLUSIONS: Increasing evidence highlights the similarities between responses of normal and cancer stem cells to signaling molecules, provided or activated by their microenvironment. While TGF-β family signaling regulates stemness of normal and cancer stem cells, its effects are diverse and depend on the cell types and physiological state of the cells. GENERAL SIGNIFICANCE: Further mechanistic studies will provide a better understanding of the roles of TGF-β family signaling in the regulation of stem cells. These basic studies may lead to the development of a new therapeutic or prognostic strategies for the treatment of cancers. This article is part of a Special Issue entitled Biochemistry of Stem Cells.
Copyright © 2012 Elsevier B.V. All rights reserved.

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Year:  2012        PMID: 22959078      PMCID: PMC4240309          DOI: 10.1016/j.bbagen.2012.08.008

Source DB:  PubMed          Journal:  Biochim Biophys Acta        ISSN: 0006-3002


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