ArticleScientific reports2019
The most common RNF43 mutant G659Vfs*41 is fully functional in inhibiting Wnt signaling and unlikely to play a role in tumorigenesis.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 64 citations in OpenAlex.
- RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.Science advances · 2026Article
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- Loss of ZNRF3/RNF43 unleashes EGFR in cancer.eLife · 2026Article
- Identification of public neoantigens with broad HLA class I coverage as candidates for off-the-shelf cancer vaccine development in colorectal cancer.Frontiers in immunology · 2026Article
- Clinical and Molecular Profiling of Colorectal Cancer: A Comprehensive Cohort Study of BRAF-Mutated Cases from a Tertiary Centre.Current oncology (Toronto, Ont.) · 2025Article
- BRAFiScience · 2025Article
- Clinical implications of Wnt pathway genetic alterations in men with advanced prostate cancer.Prostate cancer and prostatic diseases · 2025Article
- Lack of dominant-negative activity for tumor-related ZNRF3 missense mutations at endogenous levels.Oncogene · 2025Article
- Characterization of Wnt Signaling Pathway Aberrations in Metastatic Prostate Cancer.Molecular cancer research : MCR · 2024Article
- Predicting T cell receptor functionality against mutant epitopes.Cell genomics · 2024Article
- New Target(s) for RNF43 Regulation: Implications for Therapeutic Strategies.International journal of molecular sciences · 2024Review
- New insights in ubiquitin-dependent Wnt receptor regulation in tumorigenesis.In vitro cellular & developmental biology. Animal · 2024Review
- Recurrent mutations in tumor suppressorScience advances · 2024Article
- Clinical and molecular characteristics ofTherapeutic advances in medical oncology · 2024Article
- Novel insights into tumorigenesis revealed by molecular analysis of Lynch syndrome cases with multiple colorectal tumors.Frontiers in oncology · 2024Article
- MLH1 Loss in Primary Prostate Cancer.JCO precision oncology · 2023Article
- Somatic mutations can induce a noninflamed tumour microenvironment via their original gene functions, despite deriving neoantigens.British journal of cancer · 2023Article
- The tumor biological significance of RNF43 and LRP1B in gastric cancer is complex and context-dependent.Scientific reports · 2023Article
- Article
- Advances in immune checkpoint inhibitor combination strategies for microsatellite stable colorectal cancer.Frontiers in oncology · 2023Review
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7 authors at 1 institution in 1 country.
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Abstract
RNF43 is an E3 ligase that inhibits Wnt signaling by ubiquitinating Wnt receptors for degradation. It is mutated in various cancer types with the most recurrent mutation being the frameshift G659Vfs*41 with frequencies of ~5-8% in colon, stomach and endometrial cancers. This mutation, a deletion of G in a 7-G repeat, has been assumed to encode an inactive enzyme that would lead to increased Wnt signaling and drive tumorigenesis, yet no functional characterization has been reported. We analyzed the distribution of G659Vfs*41 and its association with other cancer gene mutations, and found that the mutation occurred nearly exclusively in tumors with low expression of the DNA mismatch repair gene MLH1. Mutant RNF43-G659Vfs*41 was no different from wild type RNF43 in expression, stability, localization, R-spondin binding, and inhibition of Wnt signaling. No dominant negative activity of the mutant was observed. Colon tumors with RNF43-G659Vfs*41 had low Wnt/β-catenin signaling and were frequently mutated in BRAF. A colon cancer cell line with RNF43-G659Vfs*41 and BRAF-V600E mutations was sensitive to activation of Wnt/β-catenin signaling. These findings suggest that the frequent occurrence of RNF43-G659Vfs*41 may result from error-prone replication of the 7-G repeat in MLH1-deficient tumors and that the mutation itself does not inactivate enzyme.
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