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Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells

Autophagy can protect cells while also contributing to cell damage, but the precise interplay between apoptosis and autophagy and the contribution of autophagy to cell death are still not clear. Previous studies have shown that supranutritional doses of sodium selenite promote apoptosis in human leu...

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Autores principales: Jiang, Qian, Wang, Yuhan, Li, Tianjiao, Shi, Kejian, Li, Zhushi, Ma, Yushi, Li, Feng, Luo, Hui, Yang, Yang, Xu, Caimin
Formato: Texto
Lenguaje:English
Publicado: The American Society for Cell Biology 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078072/
https://www.ncbi.nlm.nih.gov/pubmed/21346199
http://dx.doi.org/10.1091/mbc.E10-10-0860
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author Jiang, Qian
Wang, Yuhan
Li, Tianjiao
Shi, Kejian
Li, Zhushi
Ma, Yushi
Li, Feng
Luo, Hui
Yang, Yang
Xu, Caimin
author_facet Jiang, Qian
Wang, Yuhan
Li, Tianjiao
Shi, Kejian
Li, Zhushi
Ma, Yushi
Li, Feng
Luo, Hui
Yang, Yang
Xu, Caimin
author_sort Jiang, Qian
collection PubMed
description Autophagy can protect cells while also contributing to cell damage, but the precise interplay between apoptosis and autophagy and the contribution of autophagy to cell death are still not clear. Previous studies have shown that supranutritional doses of sodium selenite promote apoptosis in human leukemia NB4 cells. Here, we report that selenite treatment triggers opposite patterns of autophagy in the NB4, HL60, and Jurkat leukemia cell lines during apoptosis and provide evidence that the suppressive effect of selenite on autophagy in NB4 cells is due to the decreased expression of the chaperone protein Hsp90 (heat shock protein 90), suggesting a novel regulatory function of Hsp90 in apoptosis and autophagy. Excessive or insufficient expression indicates that Hsp90 protects NB4 cells from selenite-induced apoptosis, and selenite-induced decreases in the expression of Hsp90, especially in NB4 cells, inhibit the activities of the IκB kinase/nuclear factor-κB (IKK/NF-κB) signaling pathway, leading to less nuclear translocation and inactivation of NF-κB and the subsequent weak binding of the becn1 promoter, which facilitates the transition from autophagy to apoptosis. Taken together, our observations provide novel insights into the mechanisms underlying the balance between apoptosis and autophagy, and we also identified Hsp90–NF-κB–Beclin1 as a potential biological pathway for signaling the switch from autophagy to apoptosis in selenite-treated NB4 cells.
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spelling pubmed-30780722011-06-30 Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells Jiang, Qian Wang, Yuhan Li, Tianjiao Shi, Kejian Li, Zhushi Ma, Yushi Li, Feng Luo, Hui Yang, Yang Xu, Caimin Mol Biol Cell Articles Autophagy can protect cells while also contributing to cell damage, but the precise interplay between apoptosis and autophagy and the contribution of autophagy to cell death are still not clear. Previous studies have shown that supranutritional doses of sodium selenite promote apoptosis in human leukemia NB4 cells. Here, we report that selenite treatment triggers opposite patterns of autophagy in the NB4, HL60, and Jurkat leukemia cell lines during apoptosis and provide evidence that the suppressive effect of selenite on autophagy in NB4 cells is due to the decreased expression of the chaperone protein Hsp90 (heat shock protein 90), suggesting a novel regulatory function of Hsp90 in apoptosis and autophagy. Excessive or insufficient expression indicates that Hsp90 protects NB4 cells from selenite-induced apoptosis, and selenite-induced decreases in the expression of Hsp90, especially in NB4 cells, inhibit the activities of the IκB kinase/nuclear factor-κB (IKK/NF-κB) signaling pathway, leading to less nuclear translocation and inactivation of NF-κB and the subsequent weak binding of the becn1 promoter, which facilitates the transition from autophagy to apoptosis. Taken together, our observations provide novel insights into the mechanisms underlying the balance between apoptosis and autophagy, and we also identified Hsp90–NF-κB–Beclin1 as a potential biological pathway for signaling the switch from autophagy to apoptosis in selenite-treated NB4 cells. The American Society for Cell Biology 2011-04-15 /pmc/articles/PMC3078072/ /pubmed/21346199 http://dx.doi.org/10.1091/mbc.E10-10-0860 Text en © 2011 Jiang et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,“ “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology.
spellingShingle Articles
Jiang, Qian
Wang, Yuhan
Li, Tianjiao
Shi, Kejian
Li, Zhushi
Ma, Yushi
Li, Feng
Luo, Hui
Yang, Yang
Xu, Caimin
Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells
title Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells
title_full Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells
title_fullStr Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells
title_full_unstemmed Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells
title_short Heat shock protein 90–mediated inactivation of nuclear factor-κB switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced NB4 cells
title_sort heat shock protein 90–mediated inactivation of nuclear factor-κb switches autophagy to apoptosis through becn1 transcriptional inhibition in selenite-induced nb4 cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078072/
https://www.ncbi.nlm.nih.gov/pubmed/21346199
http://dx.doi.org/10.1091/mbc.E10-10-0860
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