HMGA2 functions as a competing endogenous RNA to promote lung cancer progression

Madhu S. Kumar, Elena Armenteros-Monterroso, Philip East, Probir Chakravorty, Nik Matthews, Monte M. Winslow and Julian Downward ()
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Madhu S. Kumar: Signal Transduction Laboratory, Cancer Research UK London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3LY, UK
Elena Armenteros-Monterroso: Signal Transduction Laboratory, Cancer Research UK London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3LY, UK
Philip East: Bioinformatics and Biostatistics Group, Cancer Research UK London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3LY, UK
Probir Chakravorty: Bioinformatics and Biostatistics Group, Cancer Research UK London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3LY, UK
Nik Matthews: Advanced Sequencing Facility, Cancer Research UK London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3LY, UK
Monte M. Winslow: the Stanford Cancer Institute, Stanford University School of Medicine
Julian Downward: Signal Transduction Laboratory, Cancer Research UK London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3LY, UK

Nature, 2014, vol. 505, issue 7482, 212-217

Abstract: HMGA2 promotes lung cancer progression in mice and humans; in mouse and human lung cancer cells, HMGA2 competes with mRNAs like TGFBR3 for the let-7 microRNA family, and in human non-small-cell lung cancer tissue, expression levels of HMGA2 and TGFBR3 are correlated, suggesting that HMGA2 functions both as a protein-coding gene and as a non-coding RNA.

Date: 2014
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DOI: 10.1038/nature12785

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