ArticleEndocrine-related cancer2012
Modulation of sodium iodide symporter expression and function by LY294002, Akti-1/2 and Rapamycin in thyroid cells.
Article in Endocrine-related cancer, 2012. 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, 39 citations in OpenAlex.
- Dedifferentiation and Redifferentiation of Follicular-Cell-Derived Thyroid Carcinoma: Mechanisms and Therapeutic Implications.Biomedicines · 2025Review
- Enhancing radioactive iodine (RAI) incorporation in RAI-refractory differentiated thyroid cancer: current insights.European thyroid journal · 2025Review
- High risk factors, molecular features and clinical management for radioactive iodine-refractory differentiated thyroid carcinoma.Frontiers in oncology · 2025Review
- Sinomenine Hydrochloride Promotes TSHR-Dependent Redifferentiation in Papillary Thyroid Cancer.International journal of molecular sciences · 2022Article
- State of the Art in the Current Management and Future Directions of Targeted Therapy for Differentiated Thyroid Cancer.International journal of molecular sciences · 2022Review
- Article
- Mechanisms of regulating NIS transport to the cell membrane and redifferentiation therapy in thyroid cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Review
- Tunicamycin as a Novel Redifferentiation Agent in Radioiodine Therapy for Anaplastic Thyroid Cancer.International journal of molecular sciences · 2021Article
- Crosstalk Between Abnormal TSHR Signaling Activation and PTEN/PI3K in the Dedifferentiation of Thyroid Cancer Cells.Frontiers in oncology · 2021Article
- Dimerization of the Sodium/Iodide Symporter.Thyroid : official journal of the American Thyroid Association · 2019Article
- Radioactive Iodine-Refractory Differentiated Thyroid Cancer and Redifferentiation Therapy.Endocrinology and metabolism (Seoul, Korea) · 2019Review
- A Nonpump Function of Sodium Iodide Symporter in Thyroid Cancer via Cross-talk with PTEN Signaling.Cancer research · 2018Article
- A somatic mutation of RasGRP3 decreases NaAmerican journal of cancer research · 2018Article
- Effects of a Phosphoinositide-3-Kinase Inhibitor on Anaplastic Thyroid Cancer Stem CellsAsian Pacific journal of cancer prevention : APJCP · 2017Article
- miRNA-106a directly targeting RARB associates with the expression of Na(+)/I(-) symporter in thyroid cancer by regulating MAPK signaling pathway.Journal of experimental & clinical cancer research : CR · 2016Article
- Somatostatin activates Ras and ERK1/2 via a G protein βγ-subunit-initiated pathway in thyroid cells.Molecular and cellular biochemistry · 2016Article
- Modulation of thyroidal radioiodide uptake by oncological pipeline inhibitors and Apigenin.Oncotarget · 2015Article
- microRNA-339-5p modulates Na+/I- symporter-mediated radioiodide uptake.Endocrine-related cancer · 2015Article
- Molecular mechanisms of 2, 3', 4, 4', 5-pentachlorobiphenyl-induced thyroid dysfunction in FRTL-5 cells.PloS one · 2015Article
- Modulation of sodium iodide symporter in thyroid cancer.Hormones & cancer · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The selective increase of Na(+)/I(-) symporter (NIS)-mediated active iodide uptake in thyroid cells allows the use of radioiodine I(131) for diagnosis and targeted treatment of thyroid cancers. However, NIS-mediated radioiodine accumulation is often reduced in thyroid cancers due to decreased NIS expression/function. As PI3K signaling is overactivated in many thyroid tumors, we investigated the effects of inhibitors for PI3K, Akt, or mTORC1 as well as their interplay on NIS modulation in thyroid cells under chronic TSH stimulation. PI3K inhibition by LY294002 increased NIS-mediated radioiodide uptake (RAIU) mainly through upregulation of NIS expression, however, mTORC1 inhibition by Rapamycin did not increase NIS-mediated RAIU despite increased NIS protein levels. In comparison, Akt inhibition by Akti-1/2 did not increase NIS protein levels, yet markedly increased NIS-mediated RAIU by decreasing iodide efflux rate and increasing iodide transport rate and iodide affinity of NIS. The effects of Akti-1/2 on NIS-mediated RAIU are not detected in nonthyroid cells, implying that Akti-1/2 or its derivatives may represent potential pharmacological reagents to selectively increase thyroidal radioiodine accumulation and therapeutic efficacy.
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