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

Chien Hsien Lai; Yu Chuan Huang; Jenq Chang Lee; Joseph Ta Chien Tseng; Kung Chao Chang; Yen Ju Chen; Nai Jhu Ding; Pao Hsuan Huang; Wen Chang Chang; Bo Wen Lin; Ruo Yu Chen; Yu Chu Wang; Yi Chien Lai; Liang Yi Hung

doi:10.1038/cddis.2016.479

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

Chien Hsien Lai
, Yu Chuan Huang
, Jenq Chang Lee
, Joseph Ta Chien Tseng
, Kung Chao Chang
, Yen Ju Chen
, Nai Jhu Ding
, Pao Hsuan Huang
, Wen Chang Chang
, Bo Wen Lin
, Ruo Yu Chen
, Yu Chu Wang
, Yi Chien Lai
, Liang Yi Hung

Research output: Contribution to journal › Article › peer-review

28 Citations (Scopus)

Abstract

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.

Original language	English
Article number	e2555
Journal	Cell Death and Disease
Volume	8
Issue number	1
DOIs	https://doi.org/10.1038/cddis.2016.479
Publication status	Published - 2017

ASJC Scopus subject areas

Immunology
Cellular and Molecular Neuroscience
Cell Biology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/cddis.2016.479

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Lai, C. H., Huang, Y. C., Lee, J. C., Tseng, J. T. C., Chang, K. C., Chen, Y. J., Ding, N. J., Huang, P. H., Chang, W. C., Lin, B. W., Chen, R. Y., Wang, Y. C., Lai, Y. C., & Hung, L. Y. (2017). Translational upregulation of Aurora-A by hnRNP Q1 contributes to cell proliferation and tumorigenesis in colorectal cancer. Cell Death and Disease, 8(1), Article e2555. https://doi.org/10.1038/cddis.2016.479

@article{970676705ebf4ba99196a8512f48c7bb,

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

abstract = "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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doi = "10.1038/cddis.2016.479",

language = "English",

volume = "8",

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AU - Lai, Chien Hsien

AU - Huang, Yu Chuan

AU - Lee, Jenq Chang

AU - Tseng, Joseph Ta Chien

AU - Chang, Kung Chao

AU - Chen, Yen Ju

AU - Ding, Nai Jhu

AU - Huang, Pao Hsuan

AU - Chang, Wen Chang

AU - Lin, Bo Wen

AU - Chen, Ruo Yu

AU - Wang, Yu Chu

AU - Lai, Yi Chien

AU - Hung, Liang Yi

PY - 2017

Y1 - 2017

N2 - 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.

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

Abstract

ASJC Scopus subject areas

UN SDGs

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