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First published online February 6, 2008

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Stressed out: thyroid cells lose contact

In a healthy cell, transmembrane and secretory proteins are folded within the ER lumen. However, ER dysfunction causes luminal protein folding to stall, triggering chaperone expression and the transient inhibition of translation, among other effects. On page 477, Bruno Di Jeso and colleagues explore a new cellular response to ER stress. The authors show that PC Cl3 thyroid cells that are treated with the ER stressors thapsigargin (TH) or tunicamycin (TN) undergo dedifferentiation – that is, they selectively downregulate thyroid-specific gene expression. Moreover, in a second thyroid cell line, treatment with TH or TN leads to lower E-cadherin levels, the formation of actin stress fibres and decreased transepithelial electrical resistance – three hallmarks of epithelial-to-mesenchymal transition. The authors go on to show that downregulation of E-cadherin and dedifferentiation are both blocked by PP2, an inhibitor of the tyrosine kinase Src. They propose a Src-dependent protective mechanism, in which the downregulation of tissue-specific genes and loss of epithelial structure promotes cell survival in the face of ER stress. These results highlight the diversity of cellular stress responses and survival tactics.

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Related articles in JCS:

ER stress is associated with dedifferentiation and an epithelial-to-mesenchymal transition-like phenotype in PC Cl3 thyroid cells

Luca Ulianich, Corrado Garbi, Antonella Sonia Treglia, Dario Punzi, Claudia Miele, Gregory Alexander Raciti, Francesco Beguinot, Eduardo Consiglio, and Bruno Di Jeso
JCS 2008 121: 477-486. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?