scholarly journals The zebrafish zic2a-zic5 gene pair acts downstream of canonical Wnt signaling to control cell proliferation in the developing tectum

Development ◽  
2007 ◽  
Vol 134 (4) ◽  
pp. 735-746 ◽  
Author(s):  
M. K. Nyholm ◽  
S.-F. Wu ◽  
R. I. Dorsky ◽  
Y. Grinblat
Keyword(s):  
Cell Proliferation ◽  
Wnt Signaling ◽  
Gene Pair ◽  
Control Cell ◽  
Canonical Wnt Signaling ◽  
Canonical Wnt

scholarly journals The Significance of the Dysregulation of Canonical Wnt Signaling in Head and Neck Squamous Cell Carcinomas

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 723 ◽  
Author(s):  
Jarosław Paluszczak
Keyword(s):  
Cell Proliferation ◽  
Head And Neck Cancer ◽  
Wnt Signaling ◽  
Head And Neck ◽  
Neck Cancer ◽  
Squamous Cell ◽  
Wnt Signaling Pathway ◽  
Squamous Cell Carcinomas ◽  
Canonical Wnt Signaling ◽  
Canonical Wnt

The knowledge about the molecular alterations which are found in head and neck squamous cell carcinomas (HNSCC) has much increased in recent years. However, we are still awaiting the translation of this knowledge to new diagnostic and therapeutic options. Among the many molecular changes that are detected in head and neck cancer, the abnormalities in several signaling pathways, which regulate cell proliferation, cell death and stemness, seem to be especially promising with regard to the development of targeted therapies. Canonical Wnt signaling is a pathway engaged in the formation of head and neck tissues, however it is not active in adult somatic mucosal cells. The aim of this review paper is to bring together significant data related to the current knowledge on the mechanisms and functional significance of the dysregulation of the Wnt/β-catenin pathway in head and neck tumors. Research evidence related to the role of Wnt signaling activation in the stimulation of cell proliferation, migration and inhibition of apoptosis in HNSCC is presented. Moreover, its role in promoting stemness traits in head and neck cancer stem-like cells is described. Evidence corroborating the hypothesis that the Wnt signaling pathway is a very promising target of novel therapeutic interventions in HNSCC is also discussed.

scholarly journals Rac1 modulates mammalian lung branching morphogenesis in part through canonical Wnt signaling

2016 ◽  
Vol 311 (6) ◽  
pp. L1036-L1049 ◽  
Author(s):  
Soula Danopoulos ◽  
Michael Krainock ◽  
Omar Toubat ◽  
Matthew Thornton ◽  
Brendan Grubbs ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wnt Signaling ◽  
Branching Morphogenesis ◽  
Mouse Lung ◽  
Canonical Wnt Signaling ◽  
Embryonic Mouse ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Canonical Wnt ◽  
Lung Branching

Lung branching morphogenesis relies on a number of factors, including proper epithelial cell proliferation and differentiation, cell polarity, and migration. Rac1, a small Rho GTPase, orchestrates a number of these cellular processes, including cell proliferation and differentiation, cellular alignment, and polarization. Furthermore, Rac1 modulates both noncanonical and canonical Wnt signaling, important pathways in lung branching morphogenesis. Culture of embryonic mouse lung explants in the presence of the Rac1 inhibitor (NSC23766) resulted in a dose-dependent decrease in branching. Increased cell death and BrdU uptake were notably seen in the mesenchyme, while no direct effect on the epithelium was observed. Moreover, vasculogenesis was impaired following Rac1 inhibition as shown by decreased Vegfa expression and impaired LacZ staining in Flk1-Lacz reporter mice. Rac1 inhibition decreased Fgf10 expression in conjunction with many of its associated factors. Moreover, using the reporter lines TOPGAL and Axin2-LacZ, there was an evident decrease in canonical Wnt signaling in the explants treated with the Rac1 inhibitor. Activation of canonical Wnt pathway using WNT3a or WNT7b only partially rescued the branching inhibition. Moreover, these results were validated on human explants, where Rac1 inhibition resulted in impaired branching and decreased AXIN2 and FGFR2b expression. We therefore conclude that Rac1 regulates lung branching morphogenesis, in part through canonical Wnt signaling. However, the exact mechanisms by which Rac1 interacts with canonical Wnt in human and mouse lung requires further investigation.

scholarly journals Ror2-mediated non-canonical Wnt signaling regulates Cdc42 and cell proliferation during tooth root development

Development ◽  
2020 ◽  
pp. dev.196360
Author(s):  
Yuanyuan Ma ◽  
Junjun Jing ◽  
Jifan Feng ◽  
Yuan Yuan ◽  
Quan Wen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wnt Signaling ◽  
Root Development ◽  
Critical Role ◽  
Canonical Wnt Signaling ◽  
Dental Tissue ◽  
Tooth Formation ◽  
Size And Shape ◽  
Dental Tissue Engineering ◽  
Canonical Wnt

The control of size and shape is an important part of regulatory process during organogenesis. Tooth formation is a highly complex process that fine-tunes the size and shape of the tooth, which are crucial for its physiological functions. Each tooth consists of a crown and one or more roots. Despite comprehensive knowledge of the mechanism that regulates early tooth crown development, we have limited understanding of the mechanism regulating root patterning and size during development. Here we show that Ror2 mediated non-canonical Wnt signaling in the dental mesenchyme plays a critical role in cell proliferation and thereby regulates root development size in mouse molars. Furthermore, Cdc42 acts as a potential downstream mediator of Ror2 signaling in root formation. Importantly, activation of Cdc42 can restore cell proliferation and partially rescue the root development size defects in Ror2 mutant mice. Collectively, our findings provide novel insights into the function of Ror2-mediated non-canonical Wnt signaling in regulating tooth morphogenesis and suggest potential avenues for dental tissue engineering.

Exendin-4 upregulates the expression of Wnt-4, a novel regulator of pancreatic β-cell proliferation

2011 ◽  
Vol 301 (5) ◽  
pp. E864-E872 ◽  
Author(s):  
Charlotte Heller ◽  
Markus C. Kühn ◽  
Birgit Mülders-Opgenoorth ◽  
Matthias Schott ◽  
Holger S. Willenberg ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
Wnt Signaling ◽  
Signaling Molecules ◽  
Antidiabetic Drugs ◽  
Canonical Wnt Signaling ◽  
Β Cells ◽  
Β Cell ◽  
Cell Functions ◽  
Canonical Wnt

The Wnt-signaling pathway regulates β-cell functions. It is not known how the expression of endogenous Wnt-signaling molecules is regulated in β-cells. Therefore, we investigated the effect of antidiabetic drugs and glucose on the expression of Wnt-signaling molecules in β-cells. Primary islets were isolated and cultured. The expression of Wnt-signaling molecules (Wnt-4, Wnt-10b, Frizzled-4, LRP5, TCF7L2) and TNFα was analyzed by semiquantitative PCR and Western blotting. Transient transfections were carried out and proliferation assays of INS-1 β-cells performed using [3H]thymidine uptake and BrdU ELISA. Insulin secretion was quantified. A knockdown (siRNA) of Wnt-4 in β-cells was carried out. Exendin-4 significantly increased the expression of Wnt-4 in β-cells on the mRNA level (2.8-fold) and the protein level (3-fold) ( P < 0.001). The effect was dose dependent, with strongest stimulation at 10 nM, and it was maintained after long-term stimulation over 4 wk. Addition of exd-(9–39), a GLP-1 receptor antagonist, abolished the effect of exendin-4. Treatment with glucose, insulin, or other antidiabetic drugs had no effect on the expression of any of the examined Wnt-signaling molecules. Functionally, Wnt-4 antagonized the activation of canonical Wnt-signaling in β-cells. Wnt-4 had no effect on glucose-stimulated insulin secretion or insulin gene expression. Knocking down Wnt-4 decreased β-cell proliferation to 45% of controls ( P < 0.05). In addition, Wnt-4 and exendin-4 treatment decreased the expression of TNFaα mRNA in primary β-cells. These data demonstrate that stimulation with exendin-4 increases the expression of Wnt-4 in β-cells. Wnt-4 modulates canonical Wnt signaling and acts as regulator of β-cell proliferation and inflammatory cytokine release. This suggests a novel mechanism through which GLP-1 can regulate β-cell proliferation.

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