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

Ulianich, Luca; Garbi, Corrado; Treglia, Antonella Sonia; Punzi, Dario; Miele, Claudia; Raciti, Gregory Alexander; Béguinot, Francesco; Consiglio, Eduardo; Jeso, Bruno Di

doi:10.1242/jcs.196584

Cited by 4 publications

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SNAI1, upregulated by ER stress, may inhibit thyroid differentiation repressing transcription of thyroid transcription factors. These results confirm the conclusions of Figures 1, 2, 4 of the paper by the same authors that were object of concerns causing the retraction of the paper (47). These results also extend previous conclusions, by showing that also the thyroid (and kidney)-specific cadherin-16 was downregulated and antioxidant genes were upregulated following ER stress.…”

supporting

confidence: 90%

Image_8.jpeg

View full text Add to dashboard Cite

supporting

confidence: 90%

Image_8.jpeg

View full text Add to dashboard Cite

ZC3H4 mediates silica-induced EndoMT via ER stress and autophagy

Jiang

Han²,

Gao³

et al. 2021

Environmental Toxicology and Pharmacology

View full text Add to dashboard Cite

The Role of the ER-Induced UPR Pathway and the Efficacy of Its Inhibitors and Inducers in the Inhibition of Tumor Progression

Walczak

Gradzik

Kabziński

et al. 2019

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Cancer is the second most frequent cause of death worldwide. It is considered to be one of the most dangerous diseases, and there is still no effective treatment for many types of cancer. Since cancerous cells have a high proliferation rate, it is pivotal for their proper functioning to have the well-functioning protein machinery. Correct protein processing and folding are crucial to maintain tumor homeostasis. Endoplasmic reticulum (ER) stress is one of the leading factors that cause disturbances in these processes. It is induced by impaired function of the ER and accumulation of unfolded proteins. Induction of ER stress affects many molecular pathways that cause the unfolded protein response (UPR). This is the way in which cells can adapt to the new conditions, but when ER stress cannot be resolved, the UPR induces cell death. The molecular mechanisms of this double-edged sword process are involved in the transition of the UPR either in a cell protection mechanism or in apoptosis. However, this process remains poorly understood but seems to be crucial in the treatment of many diseases that are related to ER stress. Hence, understanding the ER stress response, especially in the aspect of pathological consequences of UPR, has the potential to allow us to develop novel therapies and new diagnostic and prognostic markers for cancer.

show abstract

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

Cited by 4 publications

References 0 publications

Image_8.jpeg

Image_8.jpeg

ZC3H4 mediates silica-induced EndoMT via ER stress and autophagy

The Role of the ER-Induced UPR Pathway and the Efficacy of Its Inhibitors and Inducers in the Inhibition of Tumor Progression

Contact Info

Product

Resources

About