Thyroid hormone signaling in the intestinal stem cells and their niche.

Cell Mol Life Sci

Université de Strasbourg, Inserm, IRFAC/UMR-S1113, FMTS, 3 Avenue Molière 67200, Strasbourg, France.

Published: August 2022

AI Article Synopsis

  • Several studies have shown that thyroid hormones, particularly T3, play a crucial role in stem cell biology by interacting with a specific receptor called TRα1.
  • The relationship between epithelial tissues and underlying mesenchyme is essential for intestinal development and the emergence of stem cells, as demonstrated in amphibians and now being observed in mammals.
  • This review highlights how T3 and TRα1 influence both normal and cancer stem cell biology, including their metabolic regulation, expanding our understanding of their role beyond traditional signaling pathways like Wnt and Notch.

Article Abstract

Several studies emphasized the function of the thyroid hormones in stem cell biology. These hormones act through the nuclear hormone receptor TRs, which are T3-modulated transcription factors. Pioneer work on T3-dependent amphibian metamorphosis showed that the crosstalk between the epithelium and the underlying mesenchyme is absolutely required for intestinal maturation and stem cell emergence. With the recent advances of powerful animal models and 3D-organoid cultures, similar findings have now begun to be described in mammals, where the action of T3 and TRα1 control physiological and cancer-related stem cell biology. In this review, we have summarized recent findings on the multiple functions of T3 and TRα1 in intestinal epithelium stem cells, cancer stem cells and their niche. In particular, we have highlighted the regulation of metabolic functions directly linked to normal and/or cancer stem cell biology. These findings help explain other possible mechanisms by which TRα1 controls stem cell biology, beyond the more classical Wnt and Notch signaling pathways.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11072102PMC
http://dx.doi.org/10.1007/s00018-022-04503-yDOI Listing

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