ArticleEMBO reports2018
β-Catenin-RAS interaction serves as a molecular switch for RAS degradation via GSK3β.
Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Genomic and epigenomic biomarkers in colorectal cancer: From diagnosis to therapy.Advances in cancer research · 2021Pooled it
- RAS mutation status and immune microenvironment define distinct prognostic landscapes and predict chemotherapy benefit in pMMR colorectal cancer.Frontiers in immunology · 2026Article
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- Pharmacological targeting of casein kinase 1δ suppresses oncogenic NRAS-driven melanoma.Nature communications · 2024Article
- Assessment of KRASFrontiers in oncology · 2024Review
- Article
- The impact of RAS mutation on the treatment strategy of colorectal cancer.Medicine and pharmacy reports · 2023Review
- UBE2T promotes β-catenin nuclear translocation in hepatocellular carcinoma through MAPK/ERK-dependent activation.Molecular oncology · 2022Article
- Alantolactone inhibits proliferation, metastasis and promotes apoptosis of human osteosarcoma cells by suppressing Wnt/β-catenin and MAPKs signaling pathways.Genes & diseases · 2022Article
- TargetingOncoTargets and therapy · 2022Review
- Mechanistic Clues Provided by Concurrent Changes in the Expression of Genes Encoding the MFrontiers in physiology · 2022Article
- Molecular regulation after mucosal injury and regeneration in ulcerative colitis.Frontiers in molecular biosciences · 2022Review
- The Role of EREG/EGFR Pathway in Tumor Progression.International journal of molecular sciences · 2021Review
- KRAS phosphorylation regulates cell polarization and tumorigenic properties in colorectal cancer.Oncogene · 2021Article
- Targeting BRAF and RAS in Colorectal Cancer.Cancers · 2021Review
- RGL2 Drives the Metastatic Progression of Colorectal Cancer via Preventing the Protein Degradation of β-Catenin and KRAS.Cancers · 2021Article
- Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RAS proteins play critical roles in various cellular processes, including growth and transformation. RAS proteins are subjected to protein stability regulation via the Wnt/β-catenin pathway, and glycogen synthase kinase 3 beta (GSK3β) is a key player for the phosphorylation-dependent RAS degradation through proteasomes. GSK3β-mediated RAS degradation does not occur in cells that express a nondegradable mutant (MT) β-catenin. Here, we show that β-catenin directly interacts with RAS at the α-interface region that contains the GSK3β phosphorylation sites, threonine 144 and threonine 148 residues. Exposure of these sites by prior β-catenin degradation is required for RAS degradation. The introduction of a peptide that blocks the β-catenin-RAS interaction by binding to β-catenin rescues the GSK3β-mediated RAS degradation in colorectal cancer (CRC) cells that express MT β-catenin. The coregulation of β-catenin and RAS stabilities by the modulation of their interaction provides a mechanism for Wnt/β-catenin and RAS-ERK pathway cross-talk and the synergistic transformation of CRC by both
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