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Anticancer drugs

Turning cancer off

Nature Reviews Drug Discovery volume 6, page 869 (2007)Cite this article

In tumours, elevated EIF4E function results from the overexpression of EIF4E itself or increased phosphatidylinositol 3-kinase (PI3K), AKT or mammalian target of rapamycin (mTOR) signalling. The increased EIF4E function leads to the preferential enhancement of potent regulatory growth proteins such as cyclin D1, and increases ribosome loading of mRNAs that are involved in malignancy, such as MYC and vascular endothelial growth factor (VEGF).

To specifically target EIF4E the authors used ASOs, which work by recognizing and hybridizing to target mRNA to trigger ribonuclease H-mediated RNA destruction. Five 2-methoxyethyl-modified bases were attached to the ASOs to increase their potency, nuclease resistance and tissue half-life, which have been limitations of earlier generations of ASOs.

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References

ORIGINAL RESEARCH PAPER

  1. Graff, J. R. et al. Therapeutic suppression of translation initiation factor eIF4E expression reduces tumor growth without toxicity. J. Clin. Invest. 117, 2638–2648 (2007)

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FURTHER READING

  1. Hennessy, B. T. et al. Exploiting the PI3K/AKT pathway for cancer drug discovery. Nature Rev. Drug Disc. 4, 988–1004 (2005)

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Authors
  1. Man Tsuey Tse
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Tse, M. Turning cancer off. Nat Rev Drug Discov 6, 869 (2007). https://doi.org/10.1038/nrd2451

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