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

研究成果: 雜誌貢獻文章

8 引文 斯高帕斯(Scopus)

摘要

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.

原文英語
頁(從 - 到)e2555
期刊Cell death & disease
8
發行號1
DOIs
出版狀態已發佈 - 一月 12 2017

ASJC Scopus subject areas

  • Immunology
  • Cellular and Molecular Neuroscience
  • Cell Biology
  • Cancer Research

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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 & disease, 8(1), e2555. https://doi.org/10.1038/cddis.2016.479