Thyroid hormone promotes differentiation of colon cancer stem cells

被引:33
作者
Cicatiello, Annunziata Gaetana [1 ]
Ambrosio, Raffaele [2 ]
Dentice, Monica [1 ,3 ]
机构
[1] Univ Naples Federico II, Dept Clin Med & Surg, Via S Pansini 5, I-80131 Naples, Italy
[2] IRCCS SDN, Naples, Italy
[3] CEINGE Biotecnol Avanzate Scarl, Naples, Italy
基金
欧洲研究理事会;
关键词
Thyroid hormone; Deiodinases; Cancer stem cells; IODOTHYRONINE DEIODINASE EXPRESSION; TYPE-3; DEIODINASE; MOLECULAR-BASIS; RECEPTOR MUTATIONS; GENE; CARCINOMA; BETA; PROLIFERATION; CRYPT; 5-DEIODINASE;
D O I
10.1016/j.mce.2017.03.017
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Tumor formation and maintenance depend on a small fraction of cancer stem cells (CSCs) that can self-renew and generate a wide variety of differentiated cells. CSCs are resistant to chemotherapy and radiation, and can represent a reservoir of cancer cells that often cause relapse after treatment. Evidence processes suggests that CSCs also give rise to metastases. Thyroid hormone (TH) controls a variety of biological Mar including the development and functioning of most adult tissues. Recent years has seen the emergence of an intimate link between TH and multiple steps of tumorigenesis. controls the balance between the proliferation and differentiation of CSCs, and may thus be a druggable Thyroid hormone anti-cancer agent. Here, we review current understanding of the effects of TH on colorectal CSCs, including the cross regulatory loops between TH and regulators of CSC sternness. Targeting TH in the tumor microenvironment may improve treatment strategies. (C) 2017 Published by Elsevier Ireland Ltd.
引用
收藏
页码:84 / 89
页数:6
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