L1 retrotransposons, cancer stem cells and oncogenesis

Authors

  • Patricia E. Carreira,

    1. Cancer Biology Program, Mater Medical Research Institute, South Brisbane, Australia
    Search for more papers by this author
  • Sandra R. Richardson,

    1. Cancer Biology Program, Mater Medical Research Institute, South Brisbane, Australia
    Search for more papers by this author
  • Geoffrey J. Faulkner

    Corresponding author
    1. Cancer Biology Program, Mater Medical Research Institute, South Brisbane, Australia
    2. School of Biomedical Sciences, University of Queensland, Brisbane, Australia
    • G. J. Faulkner, Cancer Biology Program, Mater Medical Research Institute, South Brisbane QLD 4101, Australia

      Fax: +61 7 3443 7779

      Tel: +61 7 3443 7000

      E-mail: faulknergj@gmail.com

    Search for more papers by this author

Abstract

Retrotransposons have played a central role in human genome evolution. The accumulation of heritable L1, Alu and SVA retrotransposon insertions continues to generate structural variation within and between populations, and can result in spontaneous genetic disease. Recent works have reported somatic L1 retrotransposition in tumours, which in some cases may contribute to oncogenesis. Intriguingly, L1 mobilization appears to occur almost exclusively in cancers of epithelial cell origin. In this review, we discuss how L1 retrotransposition could potentially trigger neoplastic transformation, based on the established correlation between L1 activity and cellular plasticity, and the proven capacity of L1-mediated insertional mutagenesis to decisively alter gene expression and functional output.

Ancillary