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Updated: Feb 21, 2026

Using RNA-mediated Interference Feeding Strategy to Screen for Genes Involved in Body Size Regulation in the Nematode C. elegans
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Rnf43

Stefano Serra1, Runjan Chetty1

  • 1Department of Anatomic Pathology, Laboratory Medicine Program, University Health Network and University of Toronto, Toronto, Canada.

Journal of Clinical Pathology
|October 12, 2017
PubMed

Insights

RNF43 acts as a tumor suppressor by degrading Frizzled receptors, inhibiting Wnt/β-catenin signaling. Loss of RNF43 function enhances this pathway, and its mutations are linked to various cancers.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Signaling

Background:

  • RNF43 (E3 ubiquitin-protein ligase RNF43) is a key negative regulator of the Wnt/β-catenin signaling pathway.
  • It functions by ubiquitinating Frizzled receptors, promoting their lysosomal degradation.
  • Dysregulation of RNF43 is implicated in various human cancers.

Purpose of the Study:

  • To elucidate the structure and function of RNF43.
  • To identify and describe the most frequent mutations of RNF43 in different cancer types.
  • To understand the impact of RNF43 mutations on Wnt/β-catenin signaling.

Main Methods:

  • Structural analysis of RNF43.
  • Functional assays to assess Wnt/β-catenin pathway activity.
  • Mutation analysis in cancer patient cohorts.

Main Results:

  • RNF43's role in ubiquitinating Frizzled receptors and targeting them for degradation was confirmed.
  • Loss of RNF43 function leads to increased Frizzled stability and enhanced Wnt/β-catenin signaling.
  • Specific RNF43 mutations prevalent in various cancers were identified.

Conclusions:

  • RNF43 is a critical tumor suppressor through its regulation of Wnt/β-catenin signaling.
  • RNF43 mutations disrupt its tumor-suppressive function, contributing to oncogenesis.
  • Understanding RNF43 structure and mutations offers potential therapeutic targets in cancer.
Keywords:
cancercolorectal cancergi neoplasms pancreatic

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