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Related Concept Videos

Canonical Wnt Signaling Pathway02:54

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Cell migration, the process by which cells move from one location to another, is essential for the proper development and viability of organisms throughout their life. When cells are not able to migrate properly to their ordained locations, various disorders may occur. For example, disruption in cell migration causes chronic inflammatory diseases such as arthritis.
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The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
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Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
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Wnt5a Regulates Focal Adhesion Formation to Promote Migration in Ewing Sarcoma.

Alissa Baker1,2,3, Anusha Singhal1,2, Sarah Jacobson1,2

  • 1Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

Cancers
|November 27, 2025
PubMed
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Wnt5a signaling drives Ewing sarcoma cell migration and metastasis by altering cell adhesion and cytoskeleton. Targeting this pathway may offer new therapeutic strategies for this aggressive pediatric cancer.

Keywords:
Ewing sarcomacell adhesion moleculesmetastasisnon-canonical Wnt signaling

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Ewing sarcoma is an aggressive pediatric cancer where metastasis significantly impacts patient outcomes.
  • Previous research indicated WNT974, a Porcupine (Porcn) inhibitor, delays metastasis in Ewing sarcoma models without affecting primary tumor growth.
  • The specific role of Wnt signaling in Ewing sarcoma metastasis remained undefined.

Purpose of the Study:

  • To elucidate the role of Wnt signaling in Ewing sarcoma cell migration and metastasis.
  • To investigate the downstream molecular mechanisms affected by Wnt signaling inhibition.

Main Methods:

  • Real-time PCR to assess Wnt ligand transcription after Porcn inhibition.
  • Boyden chamber assays to quantify cell migration.
  • Western blotting, immunofluorescence, and phalloidin staining to analyze protein expression and cytoskeletal changes.
  • CRISPR-Cas9 gene editing to generate Wnt5a knockout Ewing sarcoma cell lines.

Main Results:

  • A non-canonical Wnt pathway mediated by Wnt5a was identified as a driver of Ewing sarcoma cell migration.
  • Ewing sarcoma cells exhibit feedback regulation of endogenous Wnt5a transcription in response to exogenous Wnt5a.
  • WNT974 treatment and Wnt5a knockout altered focal adhesion kinase (FAK) phosphorylation, actin cross-linking, and cell adhesion molecule (ALCAM/MCAM) modifications, impacting cell migration.
  • Wnt5a knockout cells showed impaired migration and a global loss of filamentous actin.

Conclusions:

  • Wnt5a-dependent signaling is crucial for initiating Ewing sarcoma cell migration.
  • This pathway regulates critical cytoskeletal rearrangements and cell adhesion molecule dynamics essential for the early metastatic cascade.
  • Targeting the Wnt5a pathway presents a potential therapeutic strategy for inhibiting Ewing sarcoma metastasis.