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Type I interferons induce autophagy in certain human cancer cell lines
Autophagy is an evolutionarily conserved cellular recycling mechanism that occurs at a basal level in all cells. It can be further induced by various stimuli including starvation, hypoxia, and treatment with cytokines such as IFNG/IFNγ and TGFB/TGFβ. Type I IFNs are proteins that induce an antiviral...
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/PMC3669179/ https://www.ncbi.nlm.nih.gov/pubmed/23419269 http://dx.doi.org/10.4161/auto.23921 |
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author | Schmeisser, Hana Fey, Samuel B. Horowitz, Julie Fischer, Elizabeth R. Balinsky, Corey A. Miyake, Kotaro Bekisz, Joseph Snow, Andrew L. Zoon, Kathryn C. |
author_facet | Schmeisser, Hana Fey, Samuel B. Horowitz, Julie Fischer, Elizabeth R. Balinsky, Corey A. Miyake, Kotaro Bekisz, Joseph Snow, Andrew L. Zoon, Kathryn C. |
author_sort | Schmeisser, Hana |
collection | PubMed |
description | Autophagy is an evolutionarily conserved cellular recycling mechanism that occurs at a basal level in all cells. It can be further induced by various stimuli including starvation, hypoxia, and treatment with cytokines such as IFNG/IFNγ and TGFB/TGFβ. Type I IFNs are proteins that induce an antiviral state in cells. They also have antiproliferative, proapoptotic and immunomodulatory activities. We investigated whether type I IFN can also induce autophagy in multiple human cell lines. We found that treatment with IFNA2c/IFNα2c and IFNB/IFNβ induces autophagy by 24 h in Daudi B cells, as indicated by an increase of autophagy markers MAP1LC3-II, ATG12–ATG5 complexes, and a decrease of SQSTM1 expression. An increase of MAP1LC3-II was also detected 48 h post-IFNA2c treatment in HeLa S3, MDA-MB-231, T98G and A549 cell lines. The presence of autophagosomes in selected cell lines exposed to type I IFN was confirmed by electron microscopy analysis. Increased expression of autophagy markers correlated with inhibition of MTORC1 in Daudi cells, as well as inhibition of cancer cell proliferation and changes in cell cycle progression. Concomitant blockade of either MTOR or PI3K-AKT signaling in Daudi and T98G cells treated with IFNA2c increased the level of MAP1LC3-II, indicating that the PI3K-AKT-MTORC1 signaling pathway may modulate IFN-induced autophagy in these cells. Taken together, our findings demonstrated a novel function of type I IFN as an inducer of autophagy in multiple cell lines. |
format | Online Article Text |
id | pubmed-3669179 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Landes Bioscience |
record_format | MEDLINE/PubMed |
spelling | pubmed-36691792013-06-27 Type I interferons induce autophagy in certain human cancer cell lines Schmeisser, Hana Fey, Samuel B. Horowitz, Julie Fischer, Elizabeth R. Balinsky, Corey A. Miyake, Kotaro Bekisz, Joseph Snow, Andrew L. Zoon, Kathryn C. Autophagy Basic Research Paper Autophagy is an evolutionarily conserved cellular recycling mechanism that occurs at a basal level in all cells. It can be further induced by various stimuli including starvation, hypoxia, and treatment with cytokines such as IFNG/IFNγ and TGFB/TGFβ. Type I IFNs are proteins that induce an antiviral state in cells. They also have antiproliferative, proapoptotic and immunomodulatory activities. We investigated whether type I IFN can also induce autophagy in multiple human cell lines. We found that treatment with IFNA2c/IFNα2c and IFNB/IFNβ induces autophagy by 24 h in Daudi B cells, as indicated by an increase of autophagy markers MAP1LC3-II, ATG12–ATG5 complexes, and a decrease of SQSTM1 expression. An increase of MAP1LC3-II was also detected 48 h post-IFNA2c treatment in HeLa S3, MDA-MB-231, T98G and A549 cell lines. The presence of autophagosomes in selected cell lines exposed to type I IFN was confirmed by electron microscopy analysis. Increased expression of autophagy markers correlated with inhibition of MTORC1 in Daudi cells, as well as inhibition of cancer cell proliferation and changes in cell cycle progression. Concomitant blockade of either MTOR or PI3K-AKT signaling in Daudi and T98G cells treated with IFNA2c increased the level of MAP1LC3-II, indicating that the PI3K-AKT-MTORC1 signaling pathway may modulate IFN-induced autophagy in these cells. Taken together, our findings demonstrated a novel function of type I IFN as an inducer of autophagy in multiple cell lines. Landes Bioscience 2013-05-01 2013-02-18 /pmc/articles/PMC3669179/ /pubmed/23419269 http://dx.doi.org/10.4161/auto.23921 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 | Basic Research Paper Schmeisser, Hana Fey, Samuel B. Horowitz, Julie Fischer, Elizabeth R. Balinsky, Corey A. Miyake, Kotaro Bekisz, Joseph Snow, Andrew L. Zoon, Kathryn C. Type I interferons induce autophagy in certain human cancer cell lines |
title | Type I interferons induce autophagy in certain human cancer cell lines |
title_full | Type I interferons induce autophagy in certain human cancer cell lines |
title_fullStr | Type I interferons induce autophagy in certain human cancer cell lines |
title_full_unstemmed | Type I interferons induce autophagy in certain human cancer cell lines |
title_short | Type I interferons induce autophagy in certain human cancer cell lines |
title_sort | type i interferons induce autophagy in certain human cancer cell lines |
topic | Basic Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3669179/ https://www.ncbi.nlm.nih.gov/pubmed/23419269 http://dx.doi.org/10.4161/auto.23921 |
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