Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation

Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated...
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Autor*in:	Zheng Zhang [verfasserIn] Yan Jia [verfasserIn] Feng Xv [verfasserIn] Lu-xi Song [verfasserIn] Lei Shi [verfasserIn] Juan Guo [verfasserIn] Chun-kang Chang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	myelodysplastic syndromes DEGs FOXO1 PTEN TLR4

Übergeordnetes Werk:	In: Frontiers in Genetics - Frontiers Media S.A., 2011, 11(2021)
Übergeordnetes Werk:	volume:11 ; year:2021

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fgene.2020.603956

Katalog-ID:	DOAJ055551289

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245	1	0	\|a Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation
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520			\|a Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors.
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allfields	10.3389/fgene.2020.603956 doi (DE-627)DOAJ055551289 (DE-599)DOAJ58bc858ae41d4fca99f8266dd41bf6a8 DE-627 ger DE-627 rakwb eng QH426-470 Zheng Zhang verfasserin aut Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors. myelodysplastic syndromes DEGs FOXO1 PTEN TLR4 Genetics Yan Jia verfasserin aut Feng Xv verfasserin aut Lu-xi Song verfasserin aut Lei Shi verfasserin aut Juan Guo verfasserin aut Chun-kang Chang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 11(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:11 year:2021 https://doi.org/10.3389/fgene.2020.603956 kostenfrei https://doaj.org/article/58bc858ae41d4fca99f8266dd41bf6a8 kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2020.603956/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021
spelling	10.3389/fgene.2020.603956 doi (DE-627)DOAJ055551289 (DE-599)DOAJ58bc858ae41d4fca99f8266dd41bf6a8 DE-627 ger DE-627 rakwb eng QH426-470 Zheng Zhang verfasserin aut Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors. myelodysplastic syndromes DEGs FOXO1 PTEN TLR4 Genetics Yan Jia verfasserin aut Feng Xv verfasserin aut Lu-xi Song verfasserin aut Lei Shi verfasserin aut Juan Guo verfasserin aut Chun-kang Chang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 11(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:11 year:2021 https://doi.org/10.3389/fgene.2020.603956 kostenfrei https://doaj.org/article/58bc858ae41d4fca99f8266dd41bf6a8 kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2020.603956/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021
allfields_unstemmed	10.3389/fgene.2020.603956 doi (DE-627)DOAJ055551289 (DE-599)DOAJ58bc858ae41d4fca99f8266dd41bf6a8 DE-627 ger DE-627 rakwb eng QH426-470 Zheng Zhang verfasserin aut Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors. myelodysplastic syndromes DEGs FOXO1 PTEN TLR4 Genetics Yan Jia verfasserin aut Feng Xv verfasserin aut Lu-xi Song verfasserin aut Lei Shi verfasserin aut Juan Guo verfasserin aut Chun-kang Chang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 11(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:11 year:2021 https://doi.org/10.3389/fgene.2020.603956 kostenfrei https://doaj.org/article/58bc858ae41d4fca99f8266dd41bf6a8 kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2020.603956/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021
allfieldsGer	10.3389/fgene.2020.603956 doi (DE-627)DOAJ055551289 (DE-599)DOAJ58bc858ae41d4fca99f8266dd41bf6a8 DE-627 ger DE-627 rakwb eng QH426-470 Zheng Zhang verfasserin aut Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors. myelodysplastic syndromes DEGs FOXO1 PTEN TLR4 Genetics Yan Jia verfasserin aut Feng Xv verfasserin aut Lu-xi Song verfasserin aut Lei Shi verfasserin aut Juan Guo verfasserin aut Chun-kang Chang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 11(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:11 year:2021 https://doi.org/10.3389/fgene.2020.603956 kostenfrei https://doaj.org/article/58bc858ae41d4fca99f8266dd41bf6a8 kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2020.603956/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021
allfieldsSound	10.3389/fgene.2020.603956 doi (DE-627)DOAJ055551289 (DE-599)DOAJ58bc858ae41d4fca99f8266dd41bf6a8 DE-627 ger DE-627 rakwb eng QH426-470 Zheng Zhang verfasserin aut Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors. myelodysplastic syndromes DEGs FOXO1 PTEN TLR4 Genetics Yan Jia verfasserin aut Feng Xv verfasserin aut Lu-xi Song verfasserin aut Lei Shi verfasserin aut Juan Guo verfasserin aut Chun-kang Chang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 11(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:11 year:2021 https://doi.org/10.3389/fgene.2020.603956 kostenfrei https://doaj.org/article/58bc858ae41d4fca99f8266dd41bf6a8 kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2020.603956/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2021
language	English
source	In Frontiers in Genetics 11(2021) volume:11 year:2021
sourceStr	In Frontiers in Genetics 11(2021) volume:11 year:2021
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	myelodysplastic syndromes DEGs FOXO1 PTEN TLR4 Genetics
isfreeaccess_bool	true
container_title	Frontiers in Genetics
authorswithroles_txt_mv	Zheng Zhang @@aut@@ Yan Jia @@aut@@ Feng Xv @@aut@@ Lu-xi Song @@aut@@ Lei Shi @@aut@@ Juan Guo @@aut@@ Chun-kang Chang @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
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callnumber-first	Q - Science
author	Zheng Zhang
spellingShingle	Zheng Zhang misc QH426-470 misc myelodysplastic syndromes misc DEGs misc FOXO1 misc PTEN misc TLR4 misc Genetics Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation
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topic_title	QH426-470 Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation myelodysplastic syndromes DEGs FOXO1 PTEN TLR4
topic	misc QH426-470 misc myelodysplastic syndromes misc DEGs misc FOXO1 misc PTEN misc TLR4 misc Genetics
topic_unstemmed	misc QH426-470 misc myelodysplastic syndromes misc DEGs misc FOXO1 misc PTEN misc TLR4 misc Genetics
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title	Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation
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title_full	Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation
author_sort	Zheng Zhang
journal	Frontiers in Genetics
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author_browse	Zheng Zhang Yan Jia Feng Xv Lu-xi Song Lei Shi Juan Guo Chun-kang Chang
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title_sort	decitabine induces change of biological traits in myelodysplastic syndromes via foxo1 activation
callnumber	QH426-470
title_auth	Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation
abstract	Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors.
abstractGer	Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors.
abstract_unstemmed	Decitabine (DAC) is considered to be a profound global DNA demethylation, which can induce the re-expression of silenced tumor suppressor genes. Little is known about the function of tumor suppressor gene FOXO1 in myelodysplastic syndromes (MDS). To address this issue, the study firstly investigated differentially expressed genes (DEGs) for DAC treatment in MDS cell lines, then explored the role of FOXO1 through silencing its expression before DAC treatment in MDS. The results showed that FOXO1 exists in a hyperphosphorylated, inactive form in MDS-L cells. DAC treatment both induces FOXO1 expression and reactivates the protein in its low phosphorylation level. Additionally, the results also demonstrated that this FOXO1 activation is responsible for the DAC-induced apoptosis, cell cycle arrest, antigen differentiation, and immunoregulation in MDS-L cells. We also demonstrated DAC-induced FOXO1 activation upregulates anti-tumor immune response in higher-risk MDS specimens. Collectively, these results suggest that DAC induces FOXO1 activation, which plays an important role in anti-MDS tumors.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
title_short	Decitabine Induces Change of Biological Traits in Myelodysplastic Syndromes via FOXO1 Activation
url	https://doi.org/10.3389/fgene.2020.603956 https://doaj.org/article/58bc858ae41d4fca99f8266dd41bf6a8 https://www.frontiersin.org/articles/10.3389/fgene.2020.603956/full https://doaj.org/toc/1664-8021
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