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Poster Presentation
What transposable elements are differentially translated in lung cancer?
  1. Wan R Yang1,2,
  2. Eric W Mills3,
  3. Nemanja Rodic1,
  4. Nicholas T Ingolia3,
  5. Jef D Boeke4,
  6. Hyam I Levitsky1,2 and
  7. Kathleen H Burns1,2,3
  1. Aff1 grid.21107.350000000121719311PathologyJohns Hopkins University School of Medicine Baltimore MD USA
  2. Aff2 grid.21107.350000000121719311OncologyJohns Hopkins University School of Medicine Baltimore MD USA
  3. Aff3 grid.418276.e0000000123237340EmbryologyCarnegie Institution for Science Baltimore MD USA
  4. Aff4 grid.21107.350000000121719311Molecular Biology and GeneticsJohns Hopkins University School of Medicine Baltimore MD USA

https://doi.org/10.1186/2051-1426-1-S1-P139

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    Meeting abstracts

    Transposable element (TE) expression is generally silent in somatic tissues, due to significant genomic methylation and other redundant methods of silencing. Cancer tissues, however, exhibit a marked decrease in methylation throughout the genome, which can result in de-repression of transposable element transcription. Because of this phenomenon, TEs may be tumor-specific antigens for use as potential biomarkers and vaccine targets. Lung cancer in particular is in dire need of early screening tools and treatment; the five-year survival rate is 16%. Ideal biomarkers and vaccine targets for lung cancer would be proteins or polypeptides that can be recognized by the immune system. However, TEs are subject to multiple post-transcriptional silencing mechanisms, such that increased hypomethylation does not necessarily result in increased polypeptide expression. Although evidence of increased transposable element RNAs and proteins in cancer tissues (in particular LINE-1 and HERV-K) exist in the literature, translation of other retrotransposon-encoded intermediates and other repetitive transcripts has not been thoroughly investigated. To this end we selectively sequenced translated TE sequences in a conditional mouse model of lung cancer, using ribosomal profiling. Comparing ribosomal footprints of healthy wild-type and transgenic cancerous lung tissues allows us to identify differentially translated elements.