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MYC

Splicing up your survival

Nature Reviews Cancer volume 15, page 575 (2015)Cite this article

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To identify mechanisms by which tumour cells are able to tolerate hyperactive MYC, Westbrook and colleagues had previously carried out a genome-wide short hairpin RNA (shRNA) screen in human mammary epithelial cells (HMECs) that inducibly express MYC. MYC expression and knockdown of BUD31 consistently resulted in synthetic lethality in HMECs, which underwent apoptosis, and reduced clonogenic proliferation compared with controls.

To find out more about the role of BUD31 in supporting the survival of cells with hyperactive MYC, the authors undertook immunoprecipitation of tagged BUD31 and found that several spliceosome subcomplexes were bound to it. In fact, 79 of 134 core spliceosome components were bound by BUD31, indicating that BUD31 is involved in several stages of RNA splicing. They also showed that BUD31 knockdown significantly inhibited pre-mRNA splicing in vitro and abrogated early spliceosome assembly.

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References

  1. Hsu, T. Y.-T. et al. The spliceosome is a therapeutic vulnerability in MYC-driven cancer. Nature http:/dx.doi.org/10.1038/nature14985 (2015)

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Authors
  1. Gemma K. Alderton
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Alderton, G. Splicing up your survival. Nat Rev Cancer 15, 575 (2015). https://doi.org/10.1038/nrc4013

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