ArticleOncogene2000
Ras signaling through PI3K confers hormone-independent proliferation that is compatible with differentiation.
Article in Oncogene, 2000. 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, 53 citations in OpenAlex.
- Enhancing radioactive iodine (RAI) incorporation in RAI-refractory differentiated thyroid cancer: current insights.European thyroid journal · 2025Review
- Targeting cyclin D1 as a therapeutic approach for papillary thyroid carcinoma.Frontiers in oncology · 2023Review
- Intrathyroidal feedforward and feedback network regulating thyroid hormone synthesis and secretion.Frontiers in endocrinology · 2022Review
- Novel Therapeutics in Radioactive Iodine-Resistant Thyroid Cancer.Frontiers in endocrinology · 2021Review
- Unraveling the Complex Interplay Between Transcription Factors and Signaling Molecules in Thyroid Differentiation and Function, From Embryos to Adults.Frontiers in endocrinology · 2021Review
- Fluoride Exposure Induces Inhibition of Sodium/Iodide Symporter (NIS) Contributing to Impaired Iodine Absorption and Iodine Deficiency: Molecular Mechanisms of Inhibition and Implications for Public Health.International journal of environmental research and public health · 2019Review
- Growth hormone and insulin-like growth factor 1 affect the severity of Graves' disease.Endocrinology, diabetes & metabolism case reports · 2017Article
- Switch in signaling control of mTORC1 activity after oncoprotein expression in thyroid cancer cell lines.The Journal of clinical endocrinology and metabolism · 2014Article
- Role of the ERas gene in gastric cancer cells.Oncology reports · 2013Article
- Modulation of sodium iodide symporter expression and function by LY294002, Akti-1/2 and Rapamycin in thyroid cells.Endocrine-related cancer · 2012Article
- Mutational and immunohistochemical study of the PI3K/Akt pathway in papillary thyroid carcinoma in Greece.Endocrine pathology · 2010Article
- The PI3K-Akt-mTOR pathway in initiation and progression of thyroid tumors.Molecular and cellular endocrinology · 2010Review
- The biology of the sodium iodide symporter and its potential for targeted gene delivery.Current cancer drug targets · 2010Review
- Induction of thyroid gene expression and radioiodine uptake in melanoma cells: novel therapeutic implications.PloS one · 2009Article
- Regulation of inhibitors of differentiation family proteins by thyroid-stimulating hormone in FRTL-5 thyroid cells.Journal of Korean medical science · 2008Article
- Downregulation of Rap1GAP contributes to Ras transformation.Molecular and cellular biology · 2007Article
- Mutant ras-induced proliferation of human thyroid epithelial cells requires three effector pathways.Oncogene · 2004Article
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- Immediate early genes induced by H-Ras in thyroid cells.Oncogene · 2001Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hormones are specialized mitogens that stimulate proliferation in their differentiated target cells. Thyrotropin (TSH), the physiologic regulator of thyroid cells, stimulates cAMP-mediated proliferation and thyroid-specific gene expression. The mitogenic effects of TSH require Ras, therefore Ras activation should be compatible with the maintenance of thyroid differentiation. However, expression of activated Ras extinguishes the differentiated phenotype of thyroid cells. One explanation for this apparent paradox is the selective utilization of Ras effector pathways. We tested the hypothesis that Ras signaling through PI3K mediates the mitogenic effects of TSH in cells which retain their differentiated character. Expression of a Ras effector mutant (RasV12S35) that signals preferentially through Raf-1, although sufficient to confer TSH-independent proliferation, abolished hormone-regulated expression of thyroglobulin and the sodium/iodide symporter. In contrast, expression of a Ras mutant (RasV12C40) that binds selectively to PI3K conferred TSH-independent proliferation without marked effects on thyroid-specific gene expression. Unlike the inhibitory effects of TSH on the proliferation of RasV12S35-expressing cells, TSH enhanced RasV12C40-stimulated proliferation by further increasing the activity of p70s6k, an important mediator of the mitogenic effects of TSH and RasV12C40. These results demonstrate that channeling Ras-dependent signals to PI3K confers TSH with the ability to stimulate proliferation in differentiated cells. Oncogene (2000) 19, 924 - 932.
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