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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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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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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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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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  11. Wnt, Glucocorticoid And Cellular Prion Protein Cooperate To Drive A Mesenchymal Phenotype With Poor Prognosis In Colon Cancer.

Wnt, glucocorticoid and cellular prion protein cooperate to drive a mesenchymal phenotype with poor prognosis in colon cancer.

Sophie Mouillet-Richard1,2, Angélique Gougelet3, Bruno Passet4

  • 1Centre de Recherche Des Cordeliers, INSERM, Sorbonne Université, Université Paris Cité, 75006, Paris, France. sophie.mouillet-richard@parisdescartes.fr.

Journal of Translational Medicine
|April 8, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

The Wnt-β-catenin and glucocorticoid pathways drive cellular prion protein (PrPC) expression in colorectal cancer (CRC). Targeting the PRNP-CTNNB1-NR3C1 axis may benefit patients with aggressive, mesenchymal CRC.

Keywords:
Colon cancerGlucocorticoid receptorMolecular classificationPrion protein

Related Experiment Videos

The Soft Agar Colony Formation Assay
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111.7K
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Modeling Paracrine Noncanonical Wnt Signaling In Vitro
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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Mesenchymal colorectal cancer (CRC) has a poor prognosis and high cellular prion protein (PrPC) expression.
  • PrPC is a potential therapeutic target, but its induction in CRC is not well understood.

Purpose of the Study:

  • To identify signaling pathways regulating PrPC expression in CRC.
  • To explore gene regulatory networks associated with PrPC in colorectal cancer.

Main Methods:

  • In silico analyses of CRC datasets (mouse and human).
  • ChIP-seq and promoter analyses.
  • Genetic and pharmacological manipulation of CRC cell lines and mouse models.
  • Bio-informatic analysis of clinical trial data.

Main Results:

  • Wnt-β-catenin and glucocorticoid pathways identified as upstream regulators of PRNP expression.
  • Feedback loops between PrPC and these pathways exacerbate CRC pathogenesis in mice.
  • A PRNP-CTNNB1-NR3C1 signature is overrepresented in poor-prognosis mesenchymal CRC and linked to shorter recurrence times.

Conclusions:

  • A PrPC-driven pathway is characteristic of aggressive, mesenchymal CRC.
  • Targeting the PRNP-CTNNB1-NR3C1 axis offers a potential therapeutic strategy for this CRC subtype.
Wnt-β-catenin