Upregulated transcription of ribosomal RNA genes by RNA polymerase I (Pol I) is a common feature of cancers, so Ross Hannan and colleagues tested an inhibitor of Pol I in a mouse model of lymphoma. The resultant reduction in tumour burden and increased survival in the absence of overt normal cell toxicity suggested that cancer cells might selectively rely on Pol I. Inhibition of Pol I caused a p53-dependent apoptotic response; accordingly, the cytotoxic effects on mouse and human lymphoma and leukaemia cells in vitro was greatest in p53 wild-type settings.
ORIGINAL RESEARCH PAPER
Bywater, M. J. et al. Inhibition of RNA polymerase I as a therapeutic strategy to promote cancer-specific activation of p53. Cancer Cell 22, 51–65 (2012)Article
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Burgess, D. Therapy targets ribosomal reliance. Nat Rev Cancer 12, 511 (2012). https://doi.org/10.1038/nrc3337
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DOI: https://doi.org/10.1038/nrc3337
