IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells

Abstract Background: The present study aimed to investigate the underlying role of interferon-regulatory factor 2 (IRF2)-inositol polyphosphate-4-phosphatase, type-II (INPP4B) axis in the regulation of autophagy in acute myeloid leukemia (AML) cells. Methods: Quantitative real time PCR (QRT-PCR) a...

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Autores principales:	Zhang,Feng, Li,Jiajia, Zhu,Junfeng, Liu,Lin, Zhu,Kai, Cheng,Shuang, Lv,RuDi, Zhang,Pingping
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2019
Materias:	IRF2 INPP4B Autophagy Apoptosis Acute myeloid leukemia
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100209
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spelling	oai:scielo:S0716-976020190001002092019-10-10IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cellsZhang,FengLi,JiajiaZhu,JunfengLiu,LinZhu,KaiCheng,ShuangLv,RuDiZhang,Pingping IRF2 INPP4B Autophagy Apoptosis Acute myeloid leukemia Abstract Background: The present study aimed to investigate the underlying role of interferon-regulatory factor 2 (IRF2)-inositol polyphosphate-4-phosphatase, type-II (INPP4B) axis in the regulation of autophagy in acute myeloid leukemia (AML) cells. Methods: Quantitative real time PCR (QRT-PCR) and western blot were performed to determine the expression levels of IRF2, INPP4B and autophagy-related markers in AML cell lines. Autophagy was assessed by elevated Beclin-1 expression, the conversion of light chain 3 (LC3)-I to LC3-II, downregulated p62 expression and green fluorescent protein (GFP)-LC3 puncta formation. The colony formation and apoptosis assays were performed to determine the effects of IRF2 and INPP4B on the growth of AML cells. Results: IRF2 and INPP4B were highly expressed in AML cell lines, and were positively correlated with autophagy-related proteins. Overexpression of IRF2 or INPP4B stimulated autophagy of AML cells, whereas inhibition of IRF2 or INPP4B resulted in the attenuation of autophagy. More importantly, IRF2 or INPP4B overexpression reversed autophagy inhibitor, 3-methyladenine (3-MA)-induced proliferation-inhibitory and pro-apoptotic effects, while IRF2 or INPP4B silencing overturned the proliferation-promoting and anti-apoptotic effects of autophagy activator rapamycin. Conclusion: IRF2-INPP4B signaling axis attenuated apoptosis through induction of autophagy in AML cells.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.52 20192019-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100209en10.1186/s40659-019-0218-7
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	IRF2 INPP4B Autophagy Apoptosis Acute myeloid leukemia
spellingShingle	IRF2 INPP4B Autophagy Apoptosis Acute myeloid leukemia Zhang,Feng Li,Jiajia Zhu,Junfeng Liu,Lin Zhu,Kai Cheng,Shuang Lv,RuDi Zhang,Pingping IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells
description	Abstract Background: The present study aimed to investigate the underlying role of interferon-regulatory factor 2 (IRF2)-inositol polyphosphate-4-phosphatase, type-II (INPP4B) axis in the regulation of autophagy in acute myeloid leukemia (AML) cells. Methods: Quantitative real time PCR (QRT-PCR) and western blot were performed to determine the expression levels of IRF2, INPP4B and autophagy-related markers in AML cell lines. Autophagy was assessed by elevated Beclin-1 expression, the conversion of light chain 3 (LC3)-I to LC3-II, downregulated p62 expression and green fluorescent protein (GFP)-LC3 puncta formation. The colony formation and apoptosis assays were performed to determine the effects of IRF2 and INPP4B on the growth of AML cells. Results: IRF2 and INPP4B were highly expressed in AML cell lines, and were positively correlated with autophagy-related proteins. Overexpression of IRF2 or INPP4B stimulated autophagy of AML cells, whereas inhibition of IRF2 or INPP4B resulted in the attenuation of autophagy. More importantly, IRF2 or INPP4B overexpression reversed autophagy inhibitor, 3-methyladenine (3-MA)-induced proliferation-inhibitory and pro-apoptotic effects, while IRF2 or INPP4B silencing overturned the proliferation-promoting and anti-apoptotic effects of autophagy activator rapamycin. Conclusion: IRF2-INPP4B signaling axis attenuated apoptosis through induction of autophagy in AML cells.
author	Zhang,Feng Li,Jiajia Zhu,Junfeng Liu,Lin Zhu,Kai Cheng,Shuang Lv,RuDi Zhang,Pingping
author_facet	Zhang,Feng Li,Jiajia Zhu,Junfeng Liu,Lin Zhu,Kai Cheng,Shuang Lv,RuDi Zhang,Pingping
author_sort	Zhang,Feng
title	IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells
title_short	IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells
title_full	IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells
title_fullStr	IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells
title_full_unstemmed	IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells
title_sort	irf2-inpp4b-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells
publisher	Sociedad de Biología de Chile
publishDate	2019
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602019000100209
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IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells

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