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Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer

By using RNA-immunoprecipitation assay following next-generation sequencing, a group of cell cycle-related genes targeted by hnRNP Q1 were identified, including Aurora-A kinase. Overexpressed hnRNP Q1 can upregulate Aurora-A protein, but not alter the mRNA level, through enhancing the translational...

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Autores principales: Lai, Chien-Hsien, Huang, Yu-Chuan, Lee, Jenq-Chang, Tseng, Joseph Ta-Chien, Chang, Kung-Chao, Chen, Yen-Ju, Ding, Nai-Jhu, Huang, Pao-Hsuan, Chang, Wen-Chang, Lin, Bo-Wen, Chen, Ruo-Yu, Wang, Yu-Chu, Lai, Yi-Chien, Hung, Liang-Yi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386382/
https://www.ncbi.nlm.nih.gov/pubmed/28079881
http://dx.doi.org/10.1038/cddis.2016.479
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author Lai, Chien-Hsien
Huang, Yu-Chuan
Lee, Jenq-Chang
Tseng, Joseph Ta-Chien
Chang, Kung-Chao
Chen, Yen-Ju
Ding, Nai-Jhu
Huang, Pao-Hsuan
Chang, Wen-Chang
Lin, Bo-Wen
Chen, Ruo-Yu
Wang, Yu-Chu
Lai, Yi-Chien
Hung, Liang-Yi
author_facet Lai, Chien-Hsien
Huang, Yu-Chuan
Lee, Jenq-Chang
Tseng, Joseph Ta-Chien
Chang, Kung-Chao
Chen, Yen-Ju
Ding, Nai-Jhu
Huang, Pao-Hsuan
Chang, Wen-Chang
Lin, Bo-Wen
Chen, Ruo-Yu
Wang, Yu-Chu
Lai, Yi-Chien
Hung, Liang-Yi
author_sort Lai, Chien-Hsien
collection PubMed
description By using RNA-immunoprecipitation assay following next-generation sequencing, a group of cell cycle-related genes targeted by hnRNP Q1 were identified, including Aurora-A kinase. Overexpressed hnRNP Q1 can upregulate Aurora-A protein, but not alter the mRNA level, through enhancing the translational efficiency of Aurora-A mRNA, either in a cap-dependent or -independent manner, by interacting with the 5′-UTR of Aurora-A mRNA through its RNA-binding domains (RBDs) 2 and 3. By ribosomal profiling assay further confirmed the translational regulation of Aurora-A mRNA by hnRNP Q1. Overexpression of hnRNP Q1 promotes cell proliferation and tumor growth. HnRNP Q1/ΔRBD23-truncated mutant, which loses the binding ability and translational regulation of Aurora-A mRNA, has no effect on promoting tumor growth. The expression level of hnRNP Q1 is positively correlated with Aurora-A in colorectal cancer. Taken together, our data indicate that hnRNP Q1 is a novel trans-acting factor that binds to Aurora-A mRNA 5′-UTRs and regulates its translation, which increases cell proliferation and contributes to tumorigenesis in colorectal cancer.
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spelling pubmed-53863822017-04-26 Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer Lai, Chien-Hsien Huang, Yu-Chuan Lee, Jenq-Chang Tseng, Joseph Ta-Chien Chang, Kung-Chao Chen, Yen-Ju Ding, Nai-Jhu Huang, Pao-Hsuan Chang, Wen-Chang Lin, Bo-Wen Chen, Ruo-Yu Wang, Yu-Chu Lai, Yi-Chien Hung, Liang-Yi Cell Death Dis Original Article By using RNA-immunoprecipitation assay following next-generation sequencing, a group of cell cycle-related genes targeted by hnRNP Q1 were identified, including Aurora-A kinase. Overexpressed hnRNP Q1 can upregulate Aurora-A protein, but not alter the mRNA level, through enhancing the translational efficiency of Aurora-A mRNA, either in a cap-dependent or -independent manner, by interacting with the 5′-UTR of Aurora-A mRNA through its RNA-binding domains (RBDs) 2 and 3. By ribosomal profiling assay further confirmed the translational regulation of Aurora-A mRNA by hnRNP Q1. Overexpression of hnRNP Q1 promotes cell proliferation and tumor growth. HnRNP Q1/ΔRBD23-truncated mutant, which loses the binding ability and translational regulation of Aurora-A mRNA, has no effect on promoting tumor growth. The expression level of hnRNP Q1 is positively correlated with Aurora-A in colorectal cancer. Taken together, our data indicate that hnRNP Q1 is a novel trans-acting factor that binds to Aurora-A mRNA 5′-UTRs and regulates its translation, which increases cell proliferation and contributes to tumorigenesis in colorectal cancer. Nature Publishing Group 2017-01 2017-01-12 /pmc/articles/PMC5386382/ /pubmed/28079881 http://dx.doi.org/10.1038/cddis.2016.479 Text en Copyright © 2017 The Author(s) http://creativecommons.org/licenses/by/4.0/ Cell Death and Disease is an open-access journal published by Nature Publishing Group. 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 Original Article
Lai, Chien-Hsien
Huang, Yu-Chuan
Lee, Jenq-Chang
Tseng, Joseph Ta-Chien
Chang, Kung-Chao
Chen, Yen-Ju
Ding, Nai-Jhu
Huang, Pao-Hsuan
Chang, Wen-Chang
Lin, Bo-Wen
Chen, Ruo-Yu
Wang, Yu-Chu
Lai, Yi-Chien
Hung, Liang-Yi
Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer
title Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer
title_full Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer
title_fullStr Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer
title_full_unstemmed Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer
title_short Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer
title_sort translational upregulation of aurora-a by hnrnp q1 contributes to cell proliferation and tumorigenesis in colorectal cancer
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386382/
https://www.ncbi.nlm.nih.gov/pubmed/28079881
http://dx.doi.org/10.1038/cddis.2016.479
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