Increasingly complex: New players enter the Wnt signaling network

BioEssays ◽  
2002 ◽  
Vol 24 (10) ◽  
pp. 881-884 ◽  
Author(s):  
Petra Pandur ◽  
Daniel Maurus ◽  
Michael Kühl
2019 ◽  
Vol 10 ◽  
Author(s):  
Johanna K. Ljungberg ◽  
Jessica C. Kling ◽  
Thao Thanh Tran ◽  
Antje Blumenthal

2015 ◽  
pp. 222-255
Author(s):  
Johanna Apfel ◽  
Jignesh R. Parikh ◽  
Patricia Reischmann ◽  
Rob M. Ewing ◽  
Oliver Müller ◽  
...  

BMC Biology ◽  
2016 ◽  
Vol 14 (1) ◽  
Author(s):  
Veronika Wallkamm ◽  
Karolin Rahm ◽  
Jana Schmoll ◽  
Lilian T. Kaufmann ◽  
Eva Brinkmann ◽  
...  

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Christina M Freisinger ◽  
Hilary L Griesbach ◽  
Shengda Lin ◽  
Diane C Slusarski

2004 ◽  
Vol 18 (5) ◽  
pp. 1238-1250 ◽  
Author(s):  
Takiko Daikoku ◽  
Haengseok Song ◽  
Yong Guo ◽  
Anne Riesewijk ◽  
Sietse Mosselman ◽  
...  

Abstract Successful implantation absolutely depends on the reciprocal interaction between the implantation-competent blastocyst and the receptive uterus. Expression and gene targeting studies have shown that leukemia inhibitory factor (LIF), a cytokine of the IL-6 family, and Hoxa-10, an abdominalB-like homeobox gene, are crucial to implantation and decidualization in mice. Using these mutant mice, we sought to determine the importance of Msx-1 (another homeobox gene formerly known as Hox-7.1) and of Wnt4 (a ligand of the Wnt family) signaling in implantation because of their reported functions during development. We observed that Msx-1, Wnt4, and a Wnt antagonist sFRP4 are differentially expressed in the mouse uterus during the periimplantation period, suggesting their role in implantation. In addition, we observed an aberrant uterine expression of Msx-1 and sFRP4 in Lif mutant mice, and of Wnt4 and sFRP4 in Hoxa-10 mutant mice, further reinforcing the importance of these signaling pathways in implantation. Collectively, the present results provide evidence for a novel cytokine-homeotic-Wnt signaling network in implantation.


2020 ◽  
Vol 21 (12) ◽  
pp. 4507 ◽  
Author(s):  
Boris Y. Shorning ◽  
Manisha S. Dass ◽  
Matthew J. Smalley ◽  
Helen B. Pearson

Oncogenic activation of the phosphatidylinositol-3-kinase (PI3K), protein kinase B (PKB/AKT), and mammalian target of rapamycin (mTOR) pathway is a frequent event in prostate cancer that facilitates tumor formation, disease progression and therapeutic resistance. Recent discoveries indicate that the complex crosstalk between the PI3K-AKT-mTOR pathway and multiple interacting cell signaling cascades can further promote prostate cancer progression and influence the sensitivity of prostate cancer cells to PI3K-AKT-mTOR-targeted therapies being explored in the clinic, as well as standard treatment approaches such as androgen-deprivation therapy (ADT). However, the full extent of the PI3K-AKT-mTOR signaling network during prostate tumorigenesis, invasive progression and disease recurrence remains to be determined. In this review, we outline the emerging diversity of the genetic alterations that lead to activated PI3K-AKT-mTOR signaling in prostate cancer, and discuss new mechanistic insights into the interplay between the PI3K-AKT-mTOR pathway and several key interacting oncogenic signaling cascades that can cooperate to facilitate prostate cancer growth and drug-resistance, specifically the androgen receptor (AR), mitogen-activated protein kinase (MAPK), and WNT signaling cascades. Ultimately, deepening our understanding of the broader PI3K-AKT-mTOR signaling network is crucial to aid patient stratification for PI3K-AKT-mTOR pathway-directed therapies, and to discover new therapeutic approaches for prostate cancer that improve patient outcome.


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