ArticleOncotarget2016
β-catenin signaling is required for RAS-driven thyroid cancer through PI3K activation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Signaling pathways and targeted therapy in high‑risk refractory thyroid cancer: From bench to bedside (Review).International journal of oncology · 2026Review
- Article
- KSRP-mediated Wnt/β-catenin activation promotes follicular thyroid cancer progression and stemness.British journal of cancer · 2025Article
- Oncogenic KRAS Mutations Confer a Unique Mechanotransduction Response to Peristalsis in Colorectal Cancer Cells.Molecular cancer research : MCR · 2025Article
- Tenascin-C Potentiates Wnt Signaling in Thyroid Cancer.Endocrinology · 2025Article
- Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis.Nature communications · 2024Article
- Mechanistic Insights of Thyroid Cancer Progression.Endocrinology · 2023Review
- BAMLET (Bovine α-lactalbumin made lethal to tumor cells) inhibits autophagy flux and induces apoptosis via down-regulation of protein kinase CK1α and attenuation of the AKT/p-ß-catenin (S552) pathway in RAS-mutated human colorectal HCT 116 cells.Iranian journal of basic medical sciences · 2023Article
- β-catenin attenuation leads to up-regulation of activating NKG2D ligands and tumor regression inFrontiers in immunology · 2023Article
- Article
- Molecular Landscape of Pediatric Thyroid Cancer: A Review.Diagnostics (Basel, Switzerland) · 2022Review
- Article
- Long noncoding RNA landscapes specific to benign and malignant thyroid neoplasms of distinct histological subtypes.Scientific reports · 2021Article
- Review
- Inhibition of the Wnt/β-catenin signaling pathway reduces autophagy levels in complement treated podocytes.Experimental and therapeutic medicine · 2021Article
- Galectin-3 Inhibitors Suppress Anoikis Resistance and Invasive Capacity in Thyroid Cancer Cells.International journal of endocrinology · 2021Article
- Could We Address the Interplay Between CD133, Wnt/β-Catenin, and TERT Signaling Pathways as a Potential Target for Glioblastoma Therapy?Frontiers in oncology · 2021Review
- ADAR1-mediated RNA editing is a novel oncogenic process in thyroid cancer and regulates miR-200 activity.Oncogene · 2020Article
- How does microRNA modulate Wnt/β-catenin signaling in thyroid oncogenesis?Annals of translational medicine · 2020Article
- Novel three-dimensional cultures provide insights into thyroid cancer behavior.Endocrine-related cancer · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in β-catenin are traditionally described as late events in thyroid cancer progression. However, the functional implications of β-catenin dysregulation in the context of tumor initiating events remain unclear. The aim of this work was to investigate whether the two main oncogenic drivers in thyroid cancer, RAS and BRAF, could activate the Wnt/β-catenin pathway. Expression of HRASV12 but not BRAFV600E in thyroid cells induced β-catenin nuclear localization, increased β-catenin-dependent transcriptional activity and inhibited GSK3β. In a panel of human thyroid cancer cell lines representative of the main genetic events in thyroid cancer, β-catenin activation was highly dependent on PI3K/AKT activity through its phosphorylation at S552, but not on MAPK. Silencing of β-catenin expression in cell lines led to a dramatic reduction in proliferation due to an induction of senescence, which was concordant with a reduction in tumor size in nude mice. Moreover, β-catenin silencing suppressed the expression of EMT-related genes and reduced the invasive capacity of the tumor cells. In conclusion, this work demonstrates that RAS-driven tumors induce PI3K/AKT-dependent β-catenin activation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.