Type 3 deiodinase and solid tumors: An intriguing pair

Monica Dentice, Dario Antonini, Domenico Salvatore

Research output: Contribution to journalArticle

Abstract

Introduction: Thyroid hormone (TH) metabolism is mediated by deiodinases, a family of thioredoxin fold-containing enzymes that remove iodide from thyroxine and its derivatives. The coordinated action of deiodinases allows target cells to modulate rapidly their own TH availability in response to different cues. Type 3 deiodinase (D3), the physiological inactivator of TH, is an oncofetal protein whose re-activation in adult tissues has been correlated with hyperproliferative states and with human solid tumors. This suggests a link between deiodinase-mediated TH metabolism and carcinogenesis. Areas covered: D3 is overexpressed in basal cell carcinomas (BCCs) and sustains the proliferation of BCC cells. It exerts a similar function in colon cancer, which suggests that attenuating the TH signal is part of a widespread neoplastic program. Here, recent advances in D3 research, particularly as regards the role of D3 regulation and function in solid tumors are reviewed. Expert opinion: Given the vast array of TH's physiological and cellular functions, unraveling TH metabolism in cancer biology is a promising challenge for the development of new therapies for human cancer.

Original languageEnglish
Pages (from-to)1369-1379
Number of pages11
JournalExpert Opinion on Therapeutic Targets
Volume17
Issue number11
DOIs
Publication statusPublished - Nov 2013

Fingerprint

Iodide Peroxidase
Thyroid Hormones
Tumors
Metabolism
Neoplasms
Basal Cell Carcinoma
Thioredoxins
Expert Testimony
Iodides
Thyroxine
Colonic Neoplasms
Cues
Carcinogenesis
Chemical activation
Cells
Availability
Tissue
Derivatives
Enzymes
Research

Keywords

  • Cancer
  • Deiodinase
  • Proliferation
  • Thyroid hormone

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology
  • Clinical Biochemistry
  • Molecular Medicine

Cite this

Type 3 deiodinase and solid tumors : An intriguing pair. / Dentice, Monica; Antonini, Dario; Salvatore, Domenico.

In: Expert Opinion on Therapeutic Targets, Vol. 17, No. 11, 11.2013, p. 1369-1379.

Research output: Contribution to journalArticle

Dentice, Monica ; Antonini, Dario ; Salvatore, Domenico. / Type 3 deiodinase and solid tumors : An intriguing pair. In: Expert Opinion on Therapeutic Targets. 2013 ; Vol. 17, No. 11. pp. 1369-1379.
@article{390c4a7f875f470ab3ec4e0093b92402,
title = "Type 3 deiodinase and solid tumors: An intriguing pair",
abstract = "Introduction: Thyroid hormone (TH) metabolism is mediated by deiodinases, a family of thioredoxin fold-containing enzymes that remove iodide from thyroxine and its derivatives. The coordinated action of deiodinases allows target cells to modulate rapidly their own TH availability in response to different cues. Type 3 deiodinase (D3), the physiological inactivator of TH, is an oncofetal protein whose re-activation in adult tissues has been correlated with hyperproliferative states and with human solid tumors. This suggests a link between deiodinase-mediated TH metabolism and carcinogenesis. Areas covered: D3 is overexpressed in basal cell carcinomas (BCCs) and sustains the proliferation of BCC cells. It exerts a similar function in colon cancer, which suggests that attenuating the TH signal is part of a widespread neoplastic program. Here, recent advances in D3 research, particularly as regards the role of D3 regulation and function in solid tumors are reviewed. Expert opinion: Given the vast array of TH's physiological and cellular functions, unraveling TH metabolism in cancer biology is a promising challenge for the development of new therapies for human cancer.",
keywords = "Cancer, Deiodinase, Proliferation, Thyroid hormone",
author = "Monica Dentice and Dario Antonini and Domenico Salvatore",
year = "2013",
month = "11",
doi = "10.1517/14728222.2013.833189",
language = "English",
volume = "17",
pages = "1369--1379",
journal = "Expert Opinion on Therapeutic Targets",
issn = "1472-8222",
publisher = "Informa Healthcare",
number = "11",

}

TY - JOUR

T1 - Type 3 deiodinase and solid tumors

T2 - An intriguing pair

AU - Dentice, Monica

AU - Antonini, Dario

AU - Salvatore, Domenico

PY - 2013/11

Y1 - 2013/11

N2 - Introduction: Thyroid hormone (TH) metabolism is mediated by deiodinases, a family of thioredoxin fold-containing enzymes that remove iodide from thyroxine and its derivatives. The coordinated action of deiodinases allows target cells to modulate rapidly their own TH availability in response to different cues. Type 3 deiodinase (D3), the physiological inactivator of TH, is an oncofetal protein whose re-activation in adult tissues has been correlated with hyperproliferative states and with human solid tumors. This suggests a link between deiodinase-mediated TH metabolism and carcinogenesis. Areas covered: D3 is overexpressed in basal cell carcinomas (BCCs) and sustains the proliferation of BCC cells. It exerts a similar function in colon cancer, which suggests that attenuating the TH signal is part of a widespread neoplastic program. Here, recent advances in D3 research, particularly as regards the role of D3 regulation and function in solid tumors are reviewed. Expert opinion: Given the vast array of TH's physiological and cellular functions, unraveling TH metabolism in cancer biology is a promising challenge for the development of new therapies for human cancer.

AB - Introduction: Thyroid hormone (TH) metabolism is mediated by deiodinases, a family of thioredoxin fold-containing enzymes that remove iodide from thyroxine and its derivatives. The coordinated action of deiodinases allows target cells to modulate rapidly their own TH availability in response to different cues. Type 3 deiodinase (D3), the physiological inactivator of TH, is an oncofetal protein whose re-activation in adult tissues has been correlated with hyperproliferative states and with human solid tumors. This suggests a link between deiodinase-mediated TH metabolism and carcinogenesis. Areas covered: D3 is overexpressed in basal cell carcinomas (BCCs) and sustains the proliferation of BCC cells. It exerts a similar function in colon cancer, which suggests that attenuating the TH signal is part of a widespread neoplastic program. Here, recent advances in D3 research, particularly as regards the role of D3 regulation and function in solid tumors are reviewed. Expert opinion: Given the vast array of TH's physiological and cellular functions, unraveling TH metabolism in cancer biology is a promising challenge for the development of new therapies for human cancer.

KW - Cancer

KW - Deiodinase

KW - Proliferation

KW - Thyroid hormone

UR - http://www.scopus.com/inward/record.url?scp=84886925562&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84886925562&partnerID=8YFLogxK

U2 - 10.1517/14728222.2013.833189

DO - 10.1517/14728222.2013.833189

M3 - Article

C2 - 23991650

AN - SCOPUS:84886925562

VL - 17

SP - 1369

EP - 1379

JO - Expert Opinion on Therapeutic Targets

JF - Expert Opinion on Therapeutic Targets

SN - 1472-8222

IS - 11

ER -