ArticleNeoplasia (New York, N.Y.)2014
TSH signaling overcomes B-RafV600E-induced senescence in papillary thyroid carcinogenesis through regulation of DUSP6.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- miR-451a is underexpressed and targets AKT/mTOR pathway in papillary thyroid carcinoma.Oncotarget · 2016Pooled it
- DUSP6 promotes motility, invasion, and tumorigenicity of thyroid cancer cells via IL8-induced neutrophil extracellular traps.Scientific reports · 2026Article
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- TSH suppression therapy from an individualized perspective: from mechanism to clinical decision-making.Frontiers in endocrinology · 2026Review
- ETS1 Protein Expression May Be Altered by the Complementarity of ETS1 mRNA Sequences with miR-203a-3p and miR-204-3p in Papillary Thyroid Carcinoma.International journal of molecular sciences · 2025Article
- Exploring the genetic profiles linked to senescence in thyroid tumors: insights on predicting disease progression and immune responses.Frontiers in oncology · 2025Article
- Comprehensive analysis of cellular senescence and immune microenvironment in papillary thyroid carcinoma.Aging · 2024Article
- Review
- Cellular senescence in cancer: clinical detection and prognostic implications.Journal of experimental & clinical cancer research : CR · 2022Review
- Article
- Senescent tumor cells: an overlooked adversary in the battle against cancer.Experimental & molecular medicine · 2021Review
- Lessons learned from conducting disease monitoring in low-dose exposure conditions as a counter-measure after a nuclear disaster.Journal of radiation research · 2021Review
- Lactate Dehydrogenase A as a Potential New Biomarker for Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2021Article
- The Molecular Function and Clinical Role of Thyroid Stimulating Hormone Receptor in Cancer Cells.Cells · 2020Review
- Establishment and characterization of breast cancer organoids from a patient with mammary Paget's disease.Cancer cell international · 2020Article
- Cancer Associated Fibroblasts and Senescent Thyroid Cells in the Invasive Front of Thyroid Carcinoma.Cancers · 2020Article
- Inhibition of lung cancer cells and Ras/Raf/MEK/ERK signal transduction by ectonucleoside triphosphate phosphohydrolase-7 (ENTPD7).Respiratory research · 2019Article
- Regulation of Dual-Specificity Phosphatase (DUSP) Ubiquitination and Protein Stability.International journal of molecular sciences · 2019Review
- Senescent thyrocytes and thyroid tumor cells induce M2-like macrophage polarization of human monocytes via a PGE2-dependent mechanism.Journal of experimental & clinical cancer research : CR · 2019Article
- Cellular senescence in cancer.BMB reports · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-RafV600E oncogene mutation occurs most commonly in papillary thyroid carcinoma (PTC) and is associated with tumor initiation. However, a genetic modification by B-RafV600E in thyrocytes results in oncogene-induced senescence (OIS). In the present study, we explored the factors involved in the senescence overcome program in PTC. First of all, we observed down-regulation of p-extracellular signal-regulated kinases 1/2 and up-regulation of dual specific phosphatase 6 (DUSP6) in the PTC with B-RafV600E mutation. DUSP6 overexpression in vitro induced extracellular signal-regulated kinases 1/2 dephosphorylation and inhibited B-RafV600E-induced senescence in thyrocytes. Although DUSP6 protein was degraded by B-RafV600E-induced reactive oxygen species (ROS), thyroid-stimulating hormone (TSH) stabilized DUSP6 protein by increasing Mn superoxide dismutase expression and inhibited B-RafV600E-induced senescence. Although serum TSH was not increased, its receptor was markedly upregulated in PTC with B-RafV600E. Furthermore, TSH together with DUSP6 reactivated Ras signaling, resulted in activation of Ras/AKT/glycogen synthase kinase 3β, and stabilized c-Myc protein by inhibiting its degradation. These observations led us to conclude that increased TSH signaling overcomes OIS and is essential for B-RafV600E-induced papillary thyroid carcinogenesis.
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