ArticleCancer chemotherapy and pharmacology2021
Upregulation of TRIB2 by Wnt/β-catenin activation in BRAF
Article in Cancer chemotherapy and pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Autophagy in thyroid cancer: stage-dependent switch, mutation-specific regulation, and therapeutic targeting.Oncology reviews · 2026Review
- Second-generation BRAF inhibitor Encorafenib resistance is regulated by NCOA4-mediated iron trafficking in the drug-resistant malignant melanoma cells.Scientific reports · 2025Article
- The role of tribbles homolog 2 in cell proliferation.Cell communication and signaling : CCS · 2025Review
- Review
- E-cadherin on epithelial-mesenchymal transition in thyroid cancer.Cancer cell international · 2021Review
- Novel Inhibitor-Based Therapies for Thyroid Cancer-An Update.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe BRAF
methodsTwo vemurafenib-resistant PTC cell lines (KTC1 and BCPAP) were established by continuous treatment with vemurafenib for 5 months. The knockdown and upregulation of Tribbles homolog 2 (TRIB2) in PTC cells were achieved by the transfection with short hairpin RNA against TRIB2 or recombinant lentiviral vector carrying TRIB2, respectively. The β-catenin inhibitor, ICG-001, was used for the inhibition of the Wnt/β-catenin signaling in PTC cells.
resultsVemurafenib-resistant PTC cells showed higher TRIB2 expression, upregulated ERK and AKT activation, enhanced invasive capacity, and increased epithelial-mesenchymal transition compared to the drug-sensitive groups. TRIB2 knockdown repressed the activation of ERK and AKT, inhibited invasion and EMT, and induced apoptosis of PTC cells. TRIB2 deficiency also enhanced the sensitivity of both PTC cells to vemurafenib. Vemurafenib-resistant PTC cells showed elevated expression of β-catenin in both cytoplasm and nucleus. The pre-incubation of cells with β-catenin inhibitor significantly inhibited TRIB2 expression, suppressed EMT, and repressed the activation of ERK and AKT in vemurafenib-resistant cells.
conclusionOur study showed that the upregulation of TRIB2 by the Wnt/β-catenin activation confers resistance to vemurafenib in PTC with BRAF
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Registered trials
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