Wnt and β-Catenin Signaling in the Bone Metastasis of Prostate Cancer

Wnt family proteins and β-catenin are critical for the regulation of many developmental and oncogenic processes. Wnts are secreted protein ligands which signal using a canonical pathway, and involve the transcriptional co-activator β-catenin or non-canonical pathways that are independent of β-cateni...

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Main Authors: Zachary Kaplan, Steven P. Zielske, Kristina G. Ibrahim, Frank C. Cackowski
Format: Article
Language:English
Published: MDPI AG 2021-10-01
Series:Life
Subjects:
Online Access:https://www.mdpi.com/2075-1729/11/10/1099
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author Zachary Kaplan
Steven P. Zielske
Kristina G. Ibrahim
Frank C. Cackowski
author_facet Zachary Kaplan
Steven P. Zielske
Kristina G. Ibrahim
Frank C. Cackowski
author_sort Zachary Kaplan
collection DOAJ
description Wnt family proteins and β-catenin are critical for the regulation of many developmental and oncogenic processes. Wnts are secreted protein ligands which signal using a canonical pathway, and involve the transcriptional co-activator β-catenin or non-canonical pathways that are independent of β-catenin. Bone metastasis is unfortunately a common occurrence in prostate cancer and can be conceptualized as a series of related steps or processes, most of which are regulated by Wnt ligands and/or β-catenin. At the primary tumor site, cancer cells often take on mesenchymal properties, termed epithelial mesenchymal transition (EMT), which are regulated in part by the Wnt receptor FZD4. Then, Wnt signaling, especially Wnt5A, is of importance as the cells circulate in the blood stream. Upon arriving in the bones, cancer cells migrate and take on stem-like or tumorigenic properties, as aided through Wnt or β-catenin signaling involving CHD11, CD24, and Wnt5A. Additionally, cancer cells can become dormant and evade therapy, in part due to regulation by Wnt5A. In the bones, E-selectin can aid in the reversal of EMT, a process termed mesenchymal epithelial transition (MET), as a part of metastatic tumorigenesis. Once bone tumors are established, Wnt/β-catenin signaling is involved in the suppression of osteoblast function largely through DKK1.
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spelling doaj.art-7d60676ba84c4ff99088afaad24ef7d92023-11-22T18:53:34ZengMDPI AGLife2075-17292021-10-011110109910.3390/life11101099Wnt and β-Catenin Signaling in the Bone Metastasis of Prostate CancerZachary Kaplan0Steven P. Zielske1Kristina G. Ibrahim2Frank C. Cackowski3College of Literature, Science, and the Arts, University of Michigan, Ann Arbor, MI 48109, USADepartment of Oncology and Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI 48201, USADepartment of Oncology and Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI 48201, USADepartment of Oncology and Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI 48201, USAWnt family proteins and β-catenin are critical for the regulation of many developmental and oncogenic processes. Wnts are secreted protein ligands which signal using a canonical pathway, and involve the transcriptional co-activator β-catenin or non-canonical pathways that are independent of β-catenin. Bone metastasis is unfortunately a common occurrence in prostate cancer and can be conceptualized as a series of related steps or processes, most of which are regulated by Wnt ligands and/or β-catenin. At the primary tumor site, cancer cells often take on mesenchymal properties, termed epithelial mesenchymal transition (EMT), which are regulated in part by the Wnt receptor FZD4. Then, Wnt signaling, especially Wnt5A, is of importance as the cells circulate in the blood stream. Upon arriving in the bones, cancer cells migrate and take on stem-like or tumorigenic properties, as aided through Wnt or β-catenin signaling involving CHD11, CD24, and Wnt5A. Additionally, cancer cells can become dormant and evade therapy, in part due to regulation by Wnt5A. In the bones, E-selectin can aid in the reversal of EMT, a process termed mesenchymal epithelial transition (MET), as a part of metastatic tumorigenesis. Once bone tumors are established, Wnt/β-catenin signaling is involved in the suppression of osteoblast function largely through DKK1.https://www.mdpi.com/2075-1729/11/10/1099Wntβ-cateninbone metastasisprostate cancerWnt5Abreast cancer
spellingShingle Zachary Kaplan
Steven P. Zielske
Kristina G. Ibrahim
Frank C. Cackowski
Wnt and β-Catenin Signaling in the Bone Metastasis of Prostate Cancer
Life
Wnt
β-catenin
bone metastasis
prostate cancer
Wnt5A
breast cancer
title Wnt and β-Catenin Signaling in the Bone Metastasis of Prostate Cancer
title_full Wnt and β-Catenin Signaling in the Bone Metastasis of Prostate Cancer
title_fullStr Wnt and β-Catenin Signaling in the Bone Metastasis of Prostate Cancer
title_full_unstemmed Wnt and β-Catenin Signaling in the Bone Metastasis of Prostate Cancer
title_short Wnt and β-Catenin Signaling in the Bone Metastasis of Prostate Cancer
title_sort wnt and β catenin signaling in the bone metastasis of prostate cancer
topic Wnt
β-catenin
bone metastasis
prostate cancer
Wnt5A
breast cancer
url https://www.mdpi.com/2075-1729/11/10/1099
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