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STAT3 as a new autophagy regulator
Signal transducers and activators of transcription 3 (STAT3) proteins are cytoplasmic transcription factors that translocate into the nucleus to induce transcription following growth factor or cytokine stimulation. Besides their normal functions, these proteins play an important role in cancer cells...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Landes Bioscience
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772109/ https://www.ncbi.nlm.nih.gov/pubmed/24069557 http://dx.doi.org/10.4161/jkst.24353 |
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author | Jonchère, Barbara Bélanger, Audrey Guette, Catherine Barré, Benjamin Coqueret, Olivier |
author_facet | Jonchère, Barbara Bélanger, Audrey Guette, Catherine Barré, Benjamin Coqueret, Olivier |
author_sort | Jonchère, Barbara |
collection | PubMed |
description | Signal transducers and activators of transcription 3 (STAT3) proteins are cytoplasmic transcription factors that translocate into the nucleus to induce transcription following growth factor or cytokine stimulation. Besides their normal functions, these proteins play an important role in cancer cells through the abnormal activation of cell cycle progression and the deregulation of survival and senescence pathways. New data obtained from the laboratory of Guido Kroemer identifies STAT3 as a new autophagy regulator. In the cytoplasm, in the absence of conventional phosphorylation on the tyrosine 705 residue, STAT3 interacts with the PKR kinase to inhibit eIF2A phosphorylation and so reduce autophagic pathways. This new and nonconventional function of STAT3 has an important role in normal cells but we suggest that it might also affect cancer cells and the response to chemotherapy treatment. |
format | Online Article Text |
id | pubmed-3772109 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Landes Bioscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-37721092013-09-25 STAT3 as a new autophagy regulator Jonchère, Barbara Bélanger, Audrey Guette, Catherine Barré, Benjamin Coqueret, Olivier JAKSTAT Commentary Signal transducers and activators of transcription 3 (STAT3) proteins are cytoplasmic transcription factors that translocate into the nucleus to induce transcription following growth factor or cytokine stimulation. Besides their normal functions, these proteins play an important role in cancer cells through the abnormal activation of cell cycle progression and the deregulation of survival and senescence pathways. New data obtained from the laboratory of Guido Kroemer identifies STAT3 as a new autophagy regulator. In the cytoplasm, in the absence of conventional phosphorylation on the tyrosine 705 residue, STAT3 interacts with the PKR kinase to inhibit eIF2A phosphorylation and so reduce autophagic pathways. This new and nonconventional function of STAT3 has an important role in normal cells but we suggest that it might also affect cancer cells and the response to chemotherapy treatment. Landes Bioscience 2013-07-01 2013-08-15 /pmc/articles/PMC3772109/ /pubmed/24069557 http://dx.doi.org/10.4161/jkst.24353 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Commentary Jonchère, Barbara Bélanger, Audrey Guette, Catherine Barré, Benjamin Coqueret, Olivier STAT3 as a new autophagy regulator |
title | STAT3 as a new autophagy regulator |
title_full | STAT3 as a new autophagy regulator |
title_fullStr | STAT3 as a new autophagy regulator |
title_full_unstemmed | STAT3 as a new autophagy regulator |
title_short | STAT3 as a new autophagy regulator |
title_sort | stat3 as a new autophagy regulator |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772109/ https://www.ncbi.nlm.nih.gov/pubmed/24069557 http://dx.doi.org/10.4161/jkst.24353 |
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