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Intracellular microRNA expression patterns influence cell death fates for both necrosis and apoptosis

MicroRNAs (miRNAs) are small noncoding RNA molecules that interact with target mRNAs at specific sites to induce cleavage of the mRNA or inhibit translation. Such miRNAs play a vital role in gene expression and in several other biological processes, including cell death. We have studied the mechanis...

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Autores principales: Sato, Akira, Yamamoto, Akihiro, Shimotsuma, Akira, Ogino, Yoko, Funayama, Naoki, Takahashi, Yui, Hiramoto, Akiko, Wataya, Yusuke, Kim, Hye‐Sook
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7609763/
https://www.ncbi.nlm.nih.gov/pubmed/33022895
http://dx.doi.org/10.1002/2211-5463.12995
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author Sato, Akira
Yamamoto, Akihiro
Shimotsuma, Akira
Ogino, Yoko
Funayama, Naoki
Takahashi, Yui
Hiramoto, Akiko
Wataya, Yusuke
Kim, Hye‐Sook
author_facet Sato, Akira
Yamamoto, Akihiro
Shimotsuma, Akira
Ogino, Yoko
Funayama, Naoki
Takahashi, Yui
Hiramoto, Akiko
Wataya, Yusuke
Kim, Hye‐Sook
author_sort Sato, Akira
collection PubMed
description MicroRNAs (miRNAs) are small noncoding RNA molecules that interact with target mRNAs at specific sites to induce cleavage of the mRNA or inhibit translation. Such miRNAs play a vital role in gene expression and in several other biological processes, including cell death. We have studied the mechanisms regulating cell death (necrosis in original F28‐7 cells and apoptosis in their variant F28‐7‐A cells) in the mouse mammary tumor cell line FM3A using the anticancer agent floxuridine (FUdR). We previously reported that inhibition of heat‐shock protein 90 by the specific inhibitor geldanamycin (GA) in F28‐7 cells causes a shift from necrosis to apoptosis. In this study, we investigated the intracellular miRNA expression profiles of FUdR‐treated F28‐7 cells (necrotic condition), GA plus FUdR‐treated F28‐7 cells (apoptotic condition), and FUdR‐treated F28‐7‐A cells (apoptotic condition) through miRNA microarray analysis. In addition, we knocked down Dicer, a key molecule for the expression of mature miRNAs, in F28‐7 cells to examine whether it modulates FUdR‐induced cell death. Our analysis revealed that the miRNA expression patterns differ significantly between these cell death conditions. Furthermore, we identified miRNA candidates that regulate cell death. Knockdown of Dicer in FUdR‐treated necrosis‐fated cells caused a partial shift from necrosis to apoptosis. These findings suggest that modulation of miRNA expression patterns influences the decision of cell death fate toward necrosis or apoptosis. Our findings may serve as a basis for further study of the functions of miRNAs in cell death mechanisms.
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spelling pubmed-76097632020-11-06 Intracellular microRNA expression patterns influence cell death fates for both necrosis and apoptosis Sato, Akira Yamamoto, Akihiro Shimotsuma, Akira Ogino, Yoko Funayama, Naoki Takahashi, Yui Hiramoto, Akiko Wataya, Yusuke Kim, Hye‐Sook FEBS Open Bio Research Articles MicroRNAs (miRNAs) are small noncoding RNA molecules that interact with target mRNAs at specific sites to induce cleavage of the mRNA or inhibit translation. Such miRNAs play a vital role in gene expression and in several other biological processes, including cell death. We have studied the mechanisms regulating cell death (necrosis in original F28‐7 cells and apoptosis in their variant F28‐7‐A cells) in the mouse mammary tumor cell line FM3A using the anticancer agent floxuridine (FUdR). We previously reported that inhibition of heat‐shock protein 90 by the specific inhibitor geldanamycin (GA) in F28‐7 cells causes a shift from necrosis to apoptosis. In this study, we investigated the intracellular miRNA expression profiles of FUdR‐treated F28‐7 cells (necrotic condition), GA plus FUdR‐treated F28‐7 cells (apoptotic condition), and FUdR‐treated F28‐7‐A cells (apoptotic condition) through miRNA microarray analysis. In addition, we knocked down Dicer, a key molecule for the expression of mature miRNAs, in F28‐7 cells to examine whether it modulates FUdR‐induced cell death. Our analysis revealed that the miRNA expression patterns differ significantly between these cell death conditions. Furthermore, we identified miRNA candidates that regulate cell death. Knockdown of Dicer in FUdR‐treated necrosis‐fated cells caused a partial shift from necrosis to apoptosis. These findings suggest that modulation of miRNA expression patterns influences the decision of cell death fate toward necrosis or apoptosis. Our findings may serve as a basis for further study of the functions of miRNAs in cell death mechanisms. John Wiley and Sons Inc. 2020-10-22 /pmc/articles/PMC7609763/ /pubmed/33022895 http://dx.doi.org/10.1002/2211-5463.12995 Text en © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Sato, Akira
Yamamoto, Akihiro
Shimotsuma, Akira
Ogino, Yoko
Funayama, Naoki
Takahashi, Yui
Hiramoto, Akiko
Wataya, Yusuke
Kim, Hye‐Sook
Intracellular microRNA expression patterns influence cell death fates for both necrosis and apoptosis
title Intracellular microRNA expression patterns influence cell death fates for both necrosis and apoptosis
title_full Intracellular microRNA expression patterns influence cell death fates for both necrosis and apoptosis
title_fullStr Intracellular microRNA expression patterns influence cell death fates for both necrosis and apoptosis
title_full_unstemmed Intracellular microRNA expression patterns influence cell death fates for both necrosis and apoptosis
title_short Intracellular microRNA expression patterns influence cell death fates for both necrosis and apoptosis
title_sort intracellular microrna expression patterns influence cell death fates for both necrosis and apoptosis
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7609763/
https://www.ncbi.nlm.nih.gov/pubmed/33022895
http://dx.doi.org/10.1002/2211-5463.12995
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