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Related Concept Videos

Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

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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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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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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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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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Related Experiment Video

Updated: Feb 23, 2026

Murine Prostate Micro-dissection and Surgical Castration
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WNT signalling in prostate cancer.

Virginia Murillo-Garzón1, Robert Kypta1,2

  • 1Cell Biology and Stem Cells Unit, CIC bioGUNE, Building 801A, Bizkaia Technology Park, Derio 48160, Spain.

Nature Reviews. Urology
|September 13, 2017
PubMed
Summary

Genetic and epigenetic changes in WNT signaling are crucial in prostate cancer, especially castration-resistant prostate cancer. Targeting WNT pathways shows promise for preventing cancer progression, with inhibitors in early clinical trials.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • WNT signaling pathway alterations are implicated in prostate tumor development and progression.
  • WNT signaling influences the tumor microenvironment and prostate cancer stem cells, promoting therapeutic resistance and self-renewal.
  • Genetic and epigenetic changes in WNT pathway components are observed in prostate tumors, particularly in castration-resistant prostate cancer.

Purpose of the Study:

  • To investigate the role of WNT signaling in prostate cancer, focusing on castration-resistant prostate cancer.
  • To explore the therapeutic potential of targeting WNT signaling pathways in prostate cancer.
  • To review preclinical findings on WNT signaling inhibitors for prostate cancer treatment.

Main Methods:

  • Genome sequencing and gene expression analyses of prostate tumors.
  • Preclinical studies evaluating WNT signaling inhibitors.
  • Review of existing literature on WNT pathway in prostate cancer.

Main Results:

  • WNT signaling pathway genetic and epigenetic changes are significant in prostate tumors.
  • WNT signaling promotes therapy resistance in the tumor microenvironment and cancer stem cells.
  • Preclinical studies show WNT inhibitors targeting receptor complexes or beta-catenin interactions hold therapeutic potential.

Conclusions:

  • WNT signaling is a critical factor in prostate cancer progression and castration resistance.
  • Targeting WNT signaling pathways presents a promising therapeutic strategy for prostate cancer.
  • WNT signaling inhibitors are under investigation and show potential for clinical application in prostate cancer treatment.