LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway

Abstract This study aimed to explore the role of LINC00665, miR-4458 and DOCK1 and their interactions in the development of acute myeloid leukemia (AML). The relative expression of LINC00665, miR-4458 and DOCK1 in AML samples was measured using qRT-PCR, and the protein level of DOCK1 in AML cell lin...

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Autores principales:	Xiaoyu Yang, Yan Wang, Sulei Pang, Xiaojie Li, Panpan Wang, Ruojin Ma, Yunyun Ma, Chunge Song
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ce925cd42feb47b68e4cdf6478778ae2
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spelling	oai:doaj.org-article:ce925cd42feb47b68e4cdf6478778ae22021-12-02T13:33:50ZLINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway10.1038/s41598-021-82834-92045-2322https://doaj.org/article/ce925cd42feb47b68e4cdf6478778ae22021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-82834-9https://doaj.org/toc/2045-2322Abstract This study aimed to explore the role of LINC00665, miR-4458 and DOCK1 and their interactions in the development of acute myeloid leukemia (AML). The relative expression of LINC00665, miR-4458 and DOCK1 in AML samples was measured using qRT-PCR, and the protein level of DOCK1 in AML cell lines was examined using western blot. CCK8, BrdU, transwell, cell adhesion, and caspase-3 activity assays were carried out to evaluate the viability, proliferation, migration, adhesion, and apoptosis of AML cells, respectively. Luciferase reporter, RIP, and RNA pull-down assays were also performed to confirm the target relationship among LINC00665, miR-4458 and DOCK1. Findings revealed that LINC00665 and DOCK1 were aberrantly overexpressed in AML tissues and that the expression of miR-4458 was low in AML tissues. Silencing LINC00665 or DOCK1 presented significant restriction to the proliferation, migration and adhesion of AML cells. Apart from that, it was found that inhibiting miR-4458 could enhance the proliferation, migration and adhesion of AML cells but suppress the apoptosis of AML cells. Experimental results also indicated that LINC00665 exerted its positive function on AML cells by sponging miR-4458 and that miR-4458 influenced the progression of AML cells by targeting DOCK1 directly. Overall, this finding not only provided a novel molecular pathway for the diagnosis and treatment of AML but also showed that LINC00665 could enhance the progression of AML by regulating the miR-4458/DOCK1 pathway.Xiaoyu YangYan WangSulei PangXiaojie LiPanpan WangRuojin MaYunyun MaChunge SongNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-16 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xiaoyu Yang Yan Wang Sulei Pang Xiaojie Li Panpan Wang Ruojin Ma Yunyun Ma Chunge Song LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway
description	Abstract This study aimed to explore the role of LINC00665, miR-4458 and DOCK1 and their interactions in the development of acute myeloid leukemia (AML). The relative expression of LINC00665, miR-4458 and DOCK1 in AML samples was measured using qRT-PCR, and the protein level of DOCK1 in AML cell lines was examined using western blot. CCK8, BrdU, transwell, cell adhesion, and caspase-3 activity assays were carried out to evaluate the viability, proliferation, migration, adhesion, and apoptosis of AML cells, respectively. Luciferase reporter, RIP, and RNA pull-down assays were also performed to confirm the target relationship among LINC00665, miR-4458 and DOCK1. Findings revealed that LINC00665 and DOCK1 were aberrantly overexpressed in AML tissues and that the expression of miR-4458 was low in AML tissues. Silencing LINC00665 or DOCK1 presented significant restriction to the proliferation, migration and adhesion of AML cells. Apart from that, it was found that inhibiting miR-4458 could enhance the proliferation, migration and adhesion of AML cells but suppress the apoptosis of AML cells. Experimental results also indicated that LINC00665 exerted its positive function on AML cells by sponging miR-4458 and that miR-4458 influenced the progression of AML cells by targeting DOCK1 directly. Overall, this finding not only provided a novel molecular pathway for the diagnosis and treatment of AML but also showed that LINC00665 could enhance the progression of AML by regulating the miR-4458/DOCK1 pathway.
format	article
author	Xiaoyu Yang Yan Wang Sulei Pang Xiaojie Li Panpan Wang Ruojin Ma Yunyun Ma Chunge Song
author_facet	Xiaoyu Yang Yan Wang Sulei Pang Xiaojie Li Panpan Wang Ruojin Ma Yunyun Ma Chunge Song
author_sort	Xiaoyu Yang
title	LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway
title_short	LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway
title_full	LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway
title_fullStr	LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway
title_full_unstemmed	LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway
title_sort	linc00665 promotes the progression of acute myeloid leukemia by regulating the mir-4458/dock1 pathway
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/ce925cd42feb47b68e4cdf6478778ae2
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LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway

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