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Updated: Jun 20, 2026

Colorimetric Assessment of Deiodinase 1 Activity in Human Liver Microsomes Using the Sandell-Kolthoff Reaction
Published on: April 10, 2026
Role of type 3 deiodinase in cancer
Monica Dentice1, Raffaele Ambrosio, Domenico Salvatore
1University of Naples Federico II, Department of Molecular and Clinical Endocrinology and Oncology, Via S. Pansini 5, 80131 Naples, Italy.
Abstract:
Thyroid hormone (TH) influences a wide variety of biological events in vertebrates. Among them, the balance between proliferation and differentiation is crucial in TH action in normal and pathological conditions, including cancer. Thyroid hormone signaling results from the interaction of T3 with nuclear receptors that, in concert with other transcription factors, stimulate or repress the expression of target genes, some of which are involved in the control of cellular proliferation. Ligand (T3) availability is under tight control at both extracellular and intracellular levels. Intracellular T3 concentrations are influenced by the action of selenodeiodinases. These enzymes can, within the single cell, enhance (D1 and D2) or reduce (D3) T3 concentrations, thereby constituting a potent mechanism of pre-receptoral control of TH action. Type 3 deiodinase, the major physiological inactivator of TH, is highly expressed in developing tissues and in some tumoral tissues, with a mostly unknown function. Recent studies suggest that D3 enzyme plays an important role in the control of TH metabolism and action during tumorigenesis. In this review, we focus on D3 and its potential as a novel tumoral marker and new molecular target in cancer treatment.
Insights
Type 3 deiodinase (D3) regulates thyroid hormone (TH) levels within cells. This enzyme, highly expressed in some cancers, may serve as a novel tumor marker and therapeutic target for cancer treatment.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- Thyroid hormone (TH) regulates critical cellular processes like proliferation and differentiation.
- TH signaling involves T3 interacting with nuclear receptors, influencing gene expression.
- Intracellular T3 levels are modulated by selenodeiodinases, including type 3 deiodinase (D3).
Purpose of the Study:
- To review the role of type 3 deiodinase (D3) in cancer.
- To explore D3's potential as a tumoral marker.
- To discuss D3 as a molecular target for cancer therapy.
Main Methods:
- Literature review focusing on D3 enzyme function in tumorigenesis.
- Analysis of studies investigating D3 expression in various cancer types.
- Exploration of D3's role in TH metabolism and action within tumor cells.
Main Results:
- D3 is the primary physiological inactivator of TH.
- D3 is highly expressed in certain developing and tumoral tissues.
- Emerging evidence suggests D3 significantly influences TH action during cancer development.
Conclusions:
- D3 plays a critical role in controlling TH metabolism and action in the context of cancer.
- D3's expression in tumors presents opportunities for its use as a diagnostic marker.
- Targeting D3 may offer a novel therapeutic strategy for cancer treatment.
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