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Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway
Transcriptional regulator forkhead box O (FOXO) has implications in many diverse carcinomas and often acts as a tumour suppressor. Evidence suggests that FOXO4 may play a role in cancer cell proliferation and apoptosis; however, the function and mechanism of FOXO4 on breast cancer cell growth are st...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Royal Society of Chemistry
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9070021/ https://www.ncbi.nlm.nih.gov/pubmed/35530114 http://dx.doi.org/10.1039/c9ra04380b |
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author | Qiao, Yan Wang, Bin Zhang, Huimin Yan, Yu Niu, Ligang |
author_facet | Qiao, Yan Wang, Bin Zhang, Huimin Yan, Yu Niu, Ligang |
author_sort | Qiao, Yan |
collection | PubMed |
description | Transcriptional regulator forkhead box O (FOXO) has implications in many diverse carcinomas and often acts as a tumour suppressor. Evidence suggests that FOXO4 may play a role in cancer cell proliferation and apoptosis; however, the function and mechanism of FOXO4 on breast cancer cell growth are still unknown. FOXO4 can respond to hypoxia and in the current study, our aim is to investigate the function and molecular mechanism of FOXO4 in hypoxia-induced MCF-7 cells. We first observed that hypoxia treatment reduced FOXO4 mRNA and protein expression in MCF-7 cells. Moreover, FOXO4 overexpression reversed hypoxia-induced MCF-7 cell survival. Hypoxia treatment markedly impeded MCF-7 cell apoptosis and inhibited caspase-3 activity, whereas FOXO4 overexpression promoted apoptosis and increased caspase-3 activity in hypoxia-induced MCF-7 cells. Further studies indicated that FOXO4 overexpression inhibited hypoxia-induced HIF-2α and Bnip3 expression in MCF-7 cells; moreover, FOXO4 suppressed Bnip3 expression, which is dependent on the low level of HIF-2α. Finally, we demonstrated that Bnip3 overexpression reversed the effects of FOXO4 overexpression on cell survival and apoptosis in hypoxia-induced MCF-7 cells. In conclusion, the present study suggests that FOXO4 overexpression mediated the HIF-2α/Bnip3 signal pathway, which has implications in cell survival and apoptosis in hypoxia-induced MCF-7 cells. |
format | Online Article Text |
id | pubmed-9070021 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | The Royal Society of Chemistry |
record_format | MEDLINE/PubMed |
spelling | pubmed-90700212022-05-05 Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway Qiao, Yan Wang, Bin Zhang, Huimin Yan, Yu Niu, Ligang RSC Adv Chemistry Transcriptional regulator forkhead box O (FOXO) has implications in many diverse carcinomas and often acts as a tumour suppressor. Evidence suggests that FOXO4 may play a role in cancer cell proliferation and apoptosis; however, the function and mechanism of FOXO4 on breast cancer cell growth are still unknown. FOXO4 can respond to hypoxia and in the current study, our aim is to investigate the function and molecular mechanism of FOXO4 in hypoxia-induced MCF-7 cells. We first observed that hypoxia treatment reduced FOXO4 mRNA and protein expression in MCF-7 cells. Moreover, FOXO4 overexpression reversed hypoxia-induced MCF-7 cell survival. Hypoxia treatment markedly impeded MCF-7 cell apoptosis and inhibited caspase-3 activity, whereas FOXO4 overexpression promoted apoptosis and increased caspase-3 activity in hypoxia-induced MCF-7 cells. Further studies indicated that FOXO4 overexpression inhibited hypoxia-induced HIF-2α and Bnip3 expression in MCF-7 cells; moreover, FOXO4 suppressed Bnip3 expression, which is dependent on the low level of HIF-2α. Finally, we demonstrated that Bnip3 overexpression reversed the effects of FOXO4 overexpression on cell survival and apoptosis in hypoxia-induced MCF-7 cells. In conclusion, the present study suggests that FOXO4 overexpression mediated the HIF-2α/Bnip3 signal pathway, which has implications in cell survival and apoptosis in hypoxia-induced MCF-7 cells. The Royal Society of Chemistry 2019-08-19 /pmc/articles/PMC9070021/ /pubmed/35530114 http://dx.doi.org/10.1039/c9ra04380b Text en This journal is © The Royal Society of Chemistry https://creativecommons.org/licenses/by-nc/3.0/ |
spellingShingle | Chemistry Qiao, Yan Wang, Bin Zhang, Huimin Yan, Yu Niu, Ligang Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway |
title | Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway |
title_full | Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway |
title_fullStr | Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway |
title_full_unstemmed | Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway |
title_short | Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway |
title_sort | retracted article: foxo4 overexpression suppresses hypoxia-induced-mcf-7 cell survival and promotes apoptosis through the hif-2α/bnip3 signal pathway |
topic | Chemistry |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9070021/ https://www.ncbi.nlm.nih.gov/pubmed/35530114 http://dx.doi.org/10.1039/c9ra04380b |
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