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Authors
Advisor(s)
Abstract(s)
The Sodium/Iodide Symporter (NIS) is responsible for the uptake of iodide into thyroid follicular cells, which is required for thyroid hormone production. NIS is present in most differentiated thyroid carcinoma (DTC) cells, allowing radioactive iodine (RAI) to be used to eliminate any residual disease after thyroidectomy. However, in advanced DTC, a significant proportion of metastatic lesions stop taking up iodide and become refractory to RAI therapy. This impairment of iodide uptake is mainly caused by defective functional expression of NIS, due to dysregulated transcriptional and posttranscriptional events. In this presentation, part of a Symposium entitled “Thyroid Cancer Basic: New Molecules for Better Treatments”, I will talk about how we discovered that signaling by the small GTPase RAC1 plays a crucial role in regulating NIS expression, both at the transcriptional and posttranscriptional levels, and how this might impact RAI therapy in advanced DTC.
Description
Keywords
Vias de Transdução de Sinal e Patologias Associadas Thyroid Cancer Sodium Iodide Symporter RAC1
Pedagogical Context
Citation
Publisher
Instituto Nacional de Saúde Doutor Ricardo Jorge, IP
