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Retracted Article: FOXO4 overexpression suppresses hypoxia-induced-MCF-7 cell survival and promotes apoptosis through the HIF-2α/Bnip3 signal pathway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...

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Detalles Bibliográficos
Autores principales: Qiao, Yan, Wang, Bin, Zhang, Huimin, Yan, Yu, Niu, Ligang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Royal Society of Chemistry 2019
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.
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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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