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DDX17 promotes the growth and metastasis of lung adenocarcinoma

DEAD box RNA helicase 17 (DDX17) has been shown to be an RNA binding protein involved in RNA metabolism and associated with cancer progression. However, the biological role of DDX17 in the pathogenesis of lung adenocarcinoma (LUAD) has not been well characterized. Here, we demonstrated that DDX17 pr...

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Autores principales: Liu, Xiaohui, Li, Lu, Geng, Chengjie, Wen, Shiyuan, Zhang, Cuiqiong, Deng, Chunmiao, Gao, Xuejuan, Zhang, Gong, He, Qing-yu, Liu, Langxia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9588018/
https://www.ncbi.nlm.nih.gov/pubmed/36273228
http://dx.doi.org/10.1038/s41420-022-01215-x
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author Liu, Xiaohui
Li, Lu
Geng, Chengjie
Wen, Shiyuan
Zhang, Cuiqiong
Deng, Chunmiao
Gao, Xuejuan
Zhang, Gong
He, Qing-yu
Liu, Langxia
author_facet Liu, Xiaohui
Li, Lu
Geng, Chengjie
Wen, Shiyuan
Zhang, Cuiqiong
Deng, Chunmiao
Gao, Xuejuan
Zhang, Gong
He, Qing-yu
Liu, Langxia
author_sort Liu, Xiaohui
collection PubMed
description DEAD box RNA helicase 17 (DDX17) has been shown to be an RNA binding protein involved in RNA metabolism and associated with cancer progression. However, the biological role of DDX17 in the pathogenesis of lung adenocarcinoma (LUAD) has not been well characterized. Here, we demonstrated that DDX17 promoted the proliferation, migration and invasion of H1299 and A549 lung adenocarcinoma cells. Analyses of public datasets showed that DDX17 is upregulated in LUAD specimens. Our tumor xenograft models confirmed the in vivo promoting role of DDX17 in the growth and metastasis of LUAD. Mechanistic analyses further revealed that DDX17 protein interacts with the mRNA of MYL9 and MAGEA6 and upregulates their levels. MYL9 could mediate the function of DDX17 to regulate the actin cytoskeleton rearrangement and cell adhesion, particularly by modulating the stress fiber and focal adhesion formation, whereas DDX17 might inhibit the autophagy process through MAGEA6/AMPKα1 axis in LUAD cells. Collectively, our study revealed the oncogenic role and pathways of DDX17 in LUAD.
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spelling pubmed-95880182022-10-24 DDX17 promotes the growth and metastasis of lung adenocarcinoma Liu, Xiaohui Li, Lu Geng, Chengjie Wen, Shiyuan Zhang, Cuiqiong Deng, Chunmiao Gao, Xuejuan Zhang, Gong He, Qing-yu Liu, Langxia Cell Death Discov Article DEAD box RNA helicase 17 (DDX17) has been shown to be an RNA binding protein involved in RNA metabolism and associated with cancer progression. However, the biological role of DDX17 in the pathogenesis of lung adenocarcinoma (LUAD) has not been well characterized. Here, we demonstrated that DDX17 promoted the proliferation, migration and invasion of H1299 and A549 lung adenocarcinoma cells. Analyses of public datasets showed that DDX17 is upregulated in LUAD specimens. Our tumor xenograft models confirmed the in vivo promoting role of DDX17 in the growth and metastasis of LUAD. Mechanistic analyses further revealed that DDX17 protein interacts with the mRNA of MYL9 and MAGEA6 and upregulates their levels. MYL9 could mediate the function of DDX17 to regulate the actin cytoskeleton rearrangement and cell adhesion, particularly by modulating the stress fiber and focal adhesion formation, whereas DDX17 might inhibit the autophagy process through MAGEA6/AMPKα1 axis in LUAD cells. Collectively, our study revealed the oncogenic role and pathways of DDX17 in LUAD. Nature Publishing Group UK 2022-10-22 /pmc/articles/PMC9588018/ /pubmed/36273228 http://dx.doi.org/10.1038/s41420-022-01215-x Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Liu, Xiaohui
Li, Lu
Geng, Chengjie
Wen, Shiyuan
Zhang, Cuiqiong
Deng, Chunmiao
Gao, Xuejuan
Zhang, Gong
He, Qing-yu
Liu, Langxia
DDX17 promotes the growth and metastasis of lung adenocarcinoma
title DDX17 promotes the growth and metastasis of lung adenocarcinoma
title_full DDX17 promotes the growth and metastasis of lung adenocarcinoma
title_fullStr DDX17 promotes the growth and metastasis of lung adenocarcinoma
title_full_unstemmed DDX17 promotes the growth and metastasis of lung adenocarcinoma
title_short DDX17 promotes the growth and metastasis of lung adenocarcinoma
title_sort ddx17 promotes the growth and metastasis of lung adenocarcinoma
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9588018/
https://www.ncbi.nlm.nih.gov/pubmed/36273228
http://dx.doi.org/10.1038/s41420-022-01215-x
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