PreprintCited by 3,183Wnt/β-catenin signaling in development and cancerSignaling Pathways in DiseaseHedgehog Signaling Pathway Studies

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Wnt signaling and cancer

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Polakis, Paul·2000·Genes & Development

DOI 10.1101/gad.14.15.1837

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Abstract

The regulation of cell growth and survival can be subverted by a variety of genetic defects that alter transcriptional programs normally responsible for controlling cell number. High throughput analysis of these gene expression patterns should ultimately lead to the identification of minimal expression profiles that will serve as common denominators in assigning a cancer to a given category. In the course of defining the common denominators, though, we should not be too surprised to find that cancers within a single category may nevertheless exhibit seemingly disparate genetic defects. The wnt pathway has already provided an outstanding example of this. We now know of three regulatory genes in this pathway that are mutated in primary human cancers and several others that promote experimental cancers in rodents (Fig. 1). In all of these cases the common denominator is the activation of gene transcription by -catenin. The resulting gene expression profile should provide us with a signature common to those cancers carrying defects in the wnt pathway. In this review, the wnt pathway will be covered from the perspective of cancer, with emphasis placed on molecular defects known to promote neoplastic transformation in humans and in animal models.

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“For example endostatin, which could be released from decidual collagen XVIII by EVT-mediated proteolytic cleavage, was shown to impair growth factor-induced AKT/mTOR phosphorylation and cell migration (Pollheimer et al., 2004, 2005, 2011).”
Background
Mechanism of Phosphorylation-Dependent Binding of APC to β-Catenin and Its Role in β-Catenin Degradation
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Authors: Polakis, P.
Affiliations: Genentech (US)
Corresponding author: Polakis, Paul
Venue: Genes & Development
Publisher: Cold Spring Harbor Laboratory
Published: 2000-08-01
Volume: 14
Issue: 15
Pages: 1837-1851
ISSN: 0890-9369 (ISSN-L)
1549-5477
DOI: 10.1101/gad.14.15.1837
OpenAlex: W2239090104
Cited by: 3,183
References: 190
Citations by year: 2026: 6 · 2025: 12 · 2024: 25 · 2023: 43 · 2022: 39 · 2021: 46 · 2020: 56 · 2019: 67 · 2018: 71 · 2017: 86 · 2016: 110 · 2015: 144 · 2014: 138 · 2013: 147 · 2012: 174
Type: posted content
Language: en
Open access: bronze
doi.org
Locations: Genes & Development (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Hedgehog Signaling Pathway Studies
Keywords: Wnt signaling, β-catenin, cancer, oncogenic transformation, transcriptional activation, gene expression profiles, experimental tumor model
MeSH terms: Dishevelled Proteins, Animals, Cytoskeletal Proteins, Humans, Neoplasms, Phosphoprotein Phosphatases, Phosphoproteins, Proto-Oncogene Proteins, Transcription Factors, Signal Transduction, Trans-Activators, Calcium-Calmodulin-Dependent Protein Kinases, Adenomatous Polyposis Coli Protein, Zebrafish Proteins, Glycogen Synthase Kinase 3, Adaptor Proteins, Signal Transducing, Wnt Proteins, beta Catenin

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