Cited by 11Thyroid Cancer Diagnosis and TreatmentTGF-β signaling in diseasesCancer Cells and Metastasis

Snail-1 Overexpression Correlates with Metastatic Phenotype in BRAFV600E Positive Papillary Thyroid Carcinoma

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Wieczorek-Szukala, Katarzyna, Kopczynski, Janusz, Kowalska, Aldona, Lewinski, Andrzej·2020·Journal of Clinical Medicine

Abstract

The ability of cancer to metastasize is regulated by various signaling pathways, including transforming growth factor β (TGFβ), also implicated in the upregulation of Snail-1 transcription factor in malignant neoplasms. B-type Raf kinase gene (BRAF)V600E, the most common driving mutation in papillary thyroid carcinoma (PTC), induces epithelial to mesenchymal transition (EMT) in thyroid cancer cells through changes in the Snail-1 level, increasing cell migration and invasion. However, little is known about the mechanism of Snail-1 and BRAFV600E relations in humans. Our study included 61 PTC patients with evaluated BRAFV600E mutation status. A total of 18 of those patients had lymph node metastases—of whom 10 were BRAFV600E positive, and 8 negative. Our findings indicate that the expression of Snail-1, but not TGFβ1, correlates with the metastatic phenotype in PTC. This is the first piece of evidence that the upregulation of Snail-1 corresponds with the presence of BRAFV600E mutation and increased expression of Snail-1 in metastatic PTC samples is dependent on BRAFV600E mutation status.

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  • Upregulation of pioneer developmental organizers such as SOX2, KLF4, β-catenin, SNAIL-1, c-MYC, TBX3, and BCL6 is reported downstream of BRAF/MAPK-driven tumor.

    “Even upregulation of pioneer developmental organizers, such as SOX2, KLF4, β-catenin, SNAIL-1, c-MYC, TBX3, BCL6, et al., are reported downstream of BRAF/MAPK-driven tumor, the pathways causing lineage reprogramming are not clear12,15,30–36.”

    From Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis (2024) · cites this paper as [36]

    The Discussion (page unavailable) reports higher Snail-1 expression specifically in metastatic papillary thyroid carcinomas with a BRAFV600E mutation, and suggests that the mutation may facilitate its overexpression. The paper does not report BRAF/MAPK-driven upregulation of SOX2, KLF4, β-catenin, c-MYC, TBX3, or BCL6, or establish the broader downstream relationship claimed. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Wieczorek-Szukala, K., Kopczynski, J., Kowalska, A., & Lewinski, A.
Affiliations
  • Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, 93-338 Lodz, Poland
  • Department of Pathology, Holy Cross Cancer Center, 25-734 Kielce, Poland
  • Jan Kochanowski University (PL)
Venue
Journal of Clinical Medicine
Publisher
MDPI AG
Published
2020-08-21
Volume
9
Issue
9
Pages
2701
ISSN
2077-0383 (ISSN-L)
OpenAlex
W3063492462
Cited by
11
References
1
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 3
FWCI
1.32
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Medicine (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
  • Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
Keywords
SNAI1, BRAF V600E mutation, papillary thyroid carcinoma, lymph node metastasis, epithelial-mesenchymal transition, TGF-β1, metastatic phenotype, gene overexpression, cell migration and invasion

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