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DDX59 promotes DNA replication in lung adenocarcinoma

DEAD box proteins are multifunctional proteins involved in every aspect in RNA metabolism and have essential roles in many cellular activities. Despite their importance, many DEAD box proteins remain uncharacterized. In this report, we found DDX59 overexpressed in lung adenocarcinoma. DDX59 knockdow...

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Detalles Bibliográficos
Autores principales: You, Jin, Wang, Xingshun, Wang, Jiuling, Yuan, Baolei, Zhang, Yandong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5220641/
https://www.ncbi.nlm.nih.gov/pubmed/28090355
http://dx.doi.org/10.1038/cddiscovery.2016.95
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author You, Jin
Wang, Xingshun
Wang, Jiuling
Yuan, Baolei
Zhang, Yandong
author_facet You, Jin
Wang, Xingshun
Wang, Jiuling
Yuan, Baolei
Zhang, Yandong
author_sort You, Jin
collection PubMed
description DEAD box proteins are multifunctional proteins involved in every aspect in RNA metabolism and have essential roles in many cellular activities. Despite their importance, many DEAD box proteins remain uncharacterized. In this report, we found DDX59 overexpressed in lung adenocarcinoma. DDX59 knockdown reduced cell proliferation, anchorage-independent cell growth, and caused reduction of tumor formation in immunocompromised mice. In multiple lung cancer cells, we found that DDX59 knockdown inhibits DNA synthesis; wild-type DDX59 but not helicase-defective mutant of DDX59 enhances DNA synthesis. DDX59 knockdown caused reduction of MCM protein levels, decreased the loading of MCM ring protein onto chromatin, and therefore inhibited DNA replication. Our study reveals for the first time that DDX59 has an important role in lung cancer development through promoting DNA replication.
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spelling pubmed-52206412017-01-13 DDX59 promotes DNA replication in lung adenocarcinoma You, Jin Wang, Xingshun Wang, Jiuling Yuan, Baolei Zhang, Yandong Cell Death Discov Article DEAD box proteins are multifunctional proteins involved in every aspect in RNA metabolism and have essential roles in many cellular activities. Despite their importance, many DEAD box proteins remain uncharacterized. In this report, we found DDX59 overexpressed in lung adenocarcinoma. DDX59 knockdown reduced cell proliferation, anchorage-independent cell growth, and caused reduction of tumor formation in immunocompromised mice. In multiple lung cancer cells, we found that DDX59 knockdown inhibits DNA synthesis; wild-type DDX59 but not helicase-defective mutant of DDX59 enhances DNA synthesis. DDX59 knockdown caused reduction of MCM protein levels, decreased the loading of MCM ring protein onto chromatin, and therefore inhibited DNA replication. Our study reveals for the first time that DDX59 has an important role in lung cancer development through promoting DNA replication. Nature Publishing Group 2017-01-09 /pmc/articles/PMC5220641/ /pubmed/28090355 http://dx.doi.org/10.1038/cddiscovery.2016.95 Text en Copyright © 2017 The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
You, Jin
Wang, Xingshun
Wang, Jiuling
Yuan, Baolei
Zhang, Yandong
DDX59 promotes DNA replication in lung adenocarcinoma
title DDX59 promotes DNA replication in lung adenocarcinoma
title_full DDX59 promotes DNA replication in lung adenocarcinoma
title_fullStr DDX59 promotes DNA replication in lung adenocarcinoma
title_full_unstemmed DDX59 promotes DNA replication in lung adenocarcinoma
title_short DDX59 promotes DNA replication in lung adenocarcinoma
title_sort ddx59 promotes dna replication in lung adenocarcinoma
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5220641/
https://www.ncbi.nlm.nih.gov/pubmed/28090355
http://dx.doi.org/10.1038/cddiscovery.2016.95
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