ArticleThe Journal of clinical endocrinology and metabolism2014
Follicular thyroid cancers demonstrate dual activation of PKA and mTOR as modeled by thyroid-specific deletion of Prkar1a and Pten in mice.
Article in The Journal of clinical endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Thyroid cancer: From molecular insights to therapy (Review).Oncology letters · 2025Review
- Carney Complex and Its Association With Thyroid Cancer, Molecular Pathway, and Treatment.Cureus · 2023Review
- Mouse Models to Examine Differentiated Thyroid Cancer Pathogenesis: Recent Updates.International journal of molecular sciences · 2023Review
- Preclinical Models of Follicular Cell-Derived Thyroid Cancer: An Overview from Cancer Cell Lines to Mouse Models.Endocrinology and metabolism (Seoul, Korea) · 2022Review
- Review
- Review
- miRNA-125a modulates autophagy of thyroiditis through PI3K/Akt/mTOR signaling pathway.Experimental and therapeutic medicine · 2019Article
- PKA Activates AMPK Through LKB1 Signaling in Follicular Thyroid Cancer.Frontiers in endocrinology · 2019Article
- Alterations in Sod2-Induced Oxidative Stress Affect Endocrine Cancer Progression.The Journal of clinical endocrinology and metabolism · 2018Article
- Elevated aggressive behavior in male mice with thyroid-specific Prkar1a and global Epac1 gene deletion.Hormones and behavior · 2018Article
- GLIS3 is indispensable for TSH/TSHR-dependent thyroid hormone biosynthesis and follicular cell proliferation.The Journal of clinical investigation · 2017Article
- Article
- Enhanced cAMP-stimulated protein kinase A activity in human fibrolamellar hepatocellular carcinoma.Pediatric research · 2016Article
- Obatoclax kills anaplastic thyroid cancer cells by inducing lysosome neutralization and necrosis.Oncotarget · 2016Article
- Mouse models of thyroid cancer: A 2015 update.Molecular and cellular endocrinology · 2016Review
- Fatty acid extract from CLA-enriched egg yolks can mediate transcriptome reprogramming of MCF-7 cancer cells to prevent their growth and proliferation.Genes & nutrition · 2016Article
- In Vivo Role of INPP4B in Tumor and Metastasis Suppression through Regulation of PI3K-AKT Signaling at Endosomes.Cancer discovery · 2015Article
- Neuron membrane trafficking and protein kinases involved in autism and ADHD.International journal of molecular sciences · 2015Review
- The PI3K/Akt Pathway in Tumors of Endocrine Tissues.Frontiers in endocrinology · 2015Review
- Modulation of sodium iodide symporter in thyroid cancer.Hormones & cancer · 2014Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
contextThyroid cancer is the most common form of endocrine cancer, and it is a disease whose incidence is rapidly rising. Well-differentiated epithelial thyroid cancer can be divided into papillary thyroid cancer (PTC) and follicular thyroid cancer (FTC). Although FTC is less common, patients with this condition have more frequent metastasis and a poorer prognosis than those with PTC.
objectiveThe objective of this study was to characterize the molecular mechanisms contributing to the development and metastasis of FTC.
designWe developed and characterized mice carrying thyroid-specific double knockout of the Prkar1a and Pten tumor suppressor genes and compared signaling alterations observed in the mouse FTC to the corresponding human tumors.
settingThe study was conducted at an academic research laboratory. Human samples were obtained from academic hospitals. PATIENTS: Deidentified, formalin-fixed, paraffin-embedded (FFPE) samples were analyzed from 10 control thyroids, 30 PTC cases, five follicular variant PTC cases, and 10 FTC cases.
interventionsThere were no interventions.
main outcome measuresMouse and patient samples were analyzed for expression of activated cAMP response element binding protein, AKT, ERK, and mammalian target of rapamycin (mTOR). Murine FTCs were analyzed for differential gene expression to identify genes associated with metastatic progression.
resultsDouble Prkar1a-Pten thyroid knockout mice develop FTC and recapitulate the histology and metastatic phenotype of the human disease. Analysis of signaling pathways in FTC showed that both human and mouse tumors exhibited strong activation of protein kinase A and mTOR. The development of metastatic disease was associated with the overexpression of genes required for cell movement.
conclusionsThese data imply that the protein kinase A and mTOR signaling cascades are important for the development of follicular thyroid carcinogenesis and may suggest new targets for therapeutic intervention. Mouse models paralleling the development of the stages of human FTC should provide important new tools for understanding the mechanisms of FTC development and progression and for evaluating new therapeutics.
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