ArticleCancer research2011
Proto-oncogene PBF/PTTG1IP regulates thyroid cell growth and represses radioiodide treatment.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- The effect of SLC5A5 gene expression in tumor tissues on refractoriness to radioactive iodine treatment of differentiated thyroid carcinomas.Qatar medical journal · 2025Article
- A New Twist on a Classic: Enhancing Radioiodine Uptake in Advanced Thyroid Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Combined Vorinostat and Chloroquine Inhibit Sodium-Iodide Symporter Endocytosis and Enhance Radionuclide Uptake In Vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- PTTG1IP (PBF) is a prognostic marker and correlates with immune infiltrate in ovarian cancer.American journal of translational research · 2023Article
- Redox Homeostasis in Thyroid Cancer: Implications in NaInternational journal of molecular sciences · 2022Review
- Article
- Review
- Hypoxia Constructing the Prognostic Model of Colorectal Adenocarcinoma and Related to the Immune Microenvironment.Frontiers in cell and developmental biology · 2021Article
- Radioiodine-Refractory Thyroid Cancer: Molecular Basis of Redifferentiation Therapies, Management, and Novel Therapies.Cancers · 2019Review
- PBF, a Proto-oncogene in Esophageal Carcinoma.Open medicine (Warsaw, Poland) · 2019Article
- Molecular Insights Into the Relationship Between Autoimmune Thyroid Diseases and Breast Cancer: A Critical Perspective on Autoimmunity and ER Stress.Frontiers in immunology · 2019Review
- Article
- Elevated PTTG and PBF predicts poor patient outcome and modulates DNA damage response genes in thyroid cancer.Oncogene · 2017Article
- Functional consequences of the first reported mutations of the proto-oncogene PTTG1IP/PBF.Endocrine-related cancer · 2017Article
- Pro-invasive Effect of Proto-oncogene PBF Is Modulated by an Interaction with Cortactin.The Journal of clinical endocrinology and metabolism · 2016Article
- Overexpression of Interleukin-4 in the Thyroid of Transgenic Mice Upregulates the Expression of Duox1 and the Anion Transporter Pendrin.Thyroid : official journal of the American Thyroid Association · 2016Article
- Prognostic implications of securin expression and sub-cellular localization in human breast cancer.Cellular oncology (Dordrecht, Netherlands) · 2016Article
- The PTTG1-binding factor (PBF/PTTG1IP) regulates p53 activity in thyroid cells.Endocrinology · 2014Article
- DOTS-Finder: a comprehensive tool for assessing driver genes in cancer genomes.Genome medicine · 2014Article
- Cancer: Novel target to enhance radioiodine uptake in thyroid cancer.Nature reviews. Endocrinology · 2013Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
Pituitary tumor transforming gene (PTTG)-binding factor (PBF or PTTG1IP) is a little characterized proto-oncogene that has been implicated in the etiology of breast and thyroid tumors. In this study, we created a murine transgenic model to target PBF expression to the thyroid gland (PBF-Tg mice) and found that these mice exhibited normal thyroid function, but a striking enlargement of the thyroid gland associated with hyperplastic and macrofollicular lesions. Expression of the sodium iodide symporter (NIS), a gene essential to the radioiodine ablation of thyroid hyperplasia, neoplasia, and metastasis, was also potently inhibited in PBF-Tg mice. Critically, iodide uptake was repressed in primary thyroid cultures from PBF-Tg mice, which could be rescued by PBF depletion. PBF-Tg thyroids exhibited upregulation of Akt and the TSH receptor (TSHR), each known regulators of thyrocyte proliferation, along with upregulation of the downstream proliferative marker cyclin D1. We extended and confirmed findings from the mouse model by examining PBF expression in human multinodular goiters (MNG), a hyperproliferative thyroid disorder, where PBF and TSHR was strongly upregulated relative to normal thyroid tissue. Furthermore, we showed that depleting PBF in human primary thyrocytes was sufficient to increase radioiodine uptake. Together, our findings indicate that overexpression of PBF causes thyroid cell proliferation, macrofollicular lesions, and hyperplasia, as well as repression of the critical therapeutic route for radioiodide uptake.
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