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LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway
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 ex...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7930206/ https://www.ncbi.nlm.nih.gov/pubmed/33658535 http://dx.doi.org/10.1038/s41598-021-82834-9 |
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author | Yang, Xiaoyu Wang, Yan Pang, Sulei Li, Xiaojie Wang, Panpan Ma, Ruojin Ma, Yunyun Song, Chunge |
author_facet | Yang, Xiaoyu Wang, Yan Pang, Sulei Li, Xiaojie Wang, Panpan Ma, Ruojin Ma, Yunyun Song, Chunge |
author_sort | Yang, Xiaoyu |
collection | PubMed |
description | 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 | Online Article Text |
id | pubmed-7930206 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-79302062021-03-05 LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway Yang, Xiaoyu Wang, Yan Pang, Sulei Li, Xiaojie Wang, Panpan Ma, Ruojin Ma, Yunyun Song, Chunge Sci Rep Article 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. Nature Publishing Group UK 2021-03-03 /pmc/articles/PMC7930206/ /pubmed/33658535 http://dx.doi.org/10.1038/s41598-021-82834-9 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Yang, Xiaoyu Wang, Yan Pang, Sulei Li, Xiaojie Wang, Panpan Ma, Ruojin Ma, Yunyun Song, Chunge LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway |
title | 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_short | 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 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7930206/ https://www.ncbi.nlm.nih.gov/pubmed/33658535 http://dx.doi.org/10.1038/s41598-021-82834-9 |
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