Wnt5a Signaling in Normal and Cancer Stem Cells
Joint Authors
Zhou, Yan
Kipps, Thomas J.
Zhang, Suping
Source
Issue
Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-6, 6 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2017-04-12
Country of Publication
Egypt
No. of Pages
6
Abstract EN
Wnt5a is involved in activating several noncanonical Wnt signaling pathways, which can inhibit or activate canonical Wnt/β-catenin signaling pathway in a receptor context-dependent manner.
Wnt5a signaling is critical for regulating normal developmental processes, including stem cell self-renewal, proliferation, differentiation, migration, adhesion, and polarity.
Moreover, the aberrant activation or inhibition of Wnt5a signaling is emerging as an important event in cancer progression, exerting both oncogenic and tumor suppressive effects.
Recent studies show the involvement of Wnt5a signaling in regulating normal and cancer stem cell self-renewal, cancer cell proliferation, migration, and invasion.
In this article, we review recent findings regarding the molecular mechanisms and roles of Wnt5a signaling in stem cells in embryogenesis and in the normal or neoplastic breast or ovary, highlighting that Wnt5a may have different effects on target cells depending on the surface receptors expressed by the target cell.
American Psychological Association (APA)
Zhou, Yan& Kipps, Thomas J.& Zhang, Suping. 2017. Wnt5a Signaling in Normal and Cancer Stem Cells. Stem Cells International،Vol. 2017, no. 2017, pp.1-6.
https://search.emarefa.net/detail/BIM-1201767
Modern Language Association (MLA)
Zhou, Yan…[et al.]. Wnt5a Signaling in Normal and Cancer Stem Cells. Stem Cells International No. 2017 (2017), pp.1-6.
https://search.emarefa.net/detail/BIM-1201767
American Medical Association (AMA)
Zhou, Yan& Kipps, Thomas J.& Zhang, Suping. Wnt5a Signaling in Normal and Cancer Stem Cells. Stem Cells International. 2017. Vol. 2017, no. 2017, pp.1-6.
https://search.emarefa.net/detail/BIM-1201767
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1201767