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

Author

Listed:
  • 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
    Lung Cancer Group, The Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK)

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.

Suggested Citation

  • Madhu S. Kumar & Elena Armenteros-Monterroso & Philip East & Probir Chakravorty & Nik Matthews & Monte M. Winslow & Julian Downward, 2014. "HMGA2 functions as a competing endogenous RNA to promote lung cancer progression," Nature, Nature, vol. 505(7482), pages 212-217, January.
  • Handle: RePEc:nat:nature:v:505:y:2014:i:7482:d:10.1038_nature12785
    DOI: 10.1038/nature12785
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