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Review Article Open Access
Volume 6 | Issue 1 | DOI: https://doi.org/10.46439/cancerbiology.6.079

Unleashing Wnts: Wnt ligands fuel cancer spread

  • 1Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
  • 2Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232, USA
  • 3Department of Otolaryngology-Head & Neck Surgery, Vanderbilt University Medical Center, Nashville, TN 37232, USA
  • 4Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA
  • 5Vanderbilt Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
+ Affiliations - Affiliations

Corresponding Author

Ethan Lee, ethan.lee@vanderbilt.edu

Vivian L. Weiss, Vivian.l.weiss@vumc.org

Received Date: October 29, 2025

Accepted Date: November 26, 2025

Abstract

Wnt signaling has long been implicated in cancer development, but recent studies have revealed new insights into how Wnt ligands themselves drive metastasis. Currently, research identifies Wnt1, Wnt2, Wnt2b, Wnt3, Wnt3a, Wnt4, Wnt5a, Wnt5b, Wnt6, Wnt8a, Wnt9b, Wnt10a, Wnt10b, and Wnt16 as pro-metastatic Wnt ligands, while Wnt7a, Wnt7b, Wnt8b, Wnt9a, and Wnt11 exhibit conflicting pro- and anti-metastatic roles. These ligands arise from diverse sources in the tumor microenvironment and perform a wide range of roles in the metastatic cascade, including epithelial-to-mesenchymal transition, matrix metalloproteinase production, cell motility, angiogenesis, cell death resistance, and mesenchymal-to-epithelial transition. Their diverse and critical roles in metastasis make Wnt ligands attractive therapeutic targets.

Keywords

Wnt, Metastasis, Wnt/β-catenin signaling, EMT, Angiogenesis, Cancer therapeutics

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