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Crippling SWI-SNF makes tumors GLI-ful

Nature Medicine volume 16, pages 1374–1376 (2010)Cite this article

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The chromatin remodeling complex SWI-SNF is altered in cancer. New findings now show that the core component SNF5 can block a Hedgehog (Hh) effector, which promotes malignant rhabdoid tumor growth when SNF5 is lost (pages 1429–1433). Targeting this Hh effector may be a way to combat these aggressive childhood tumors.

Most of our DNA is wrapped around histone-based nucleosomes and packaged into chromatin. Nucleosomes control the access of molecular machines to our DNA, affecting diverse aspects of gene function, such as replication, repair and transcriptional regulation. Given the relevance of chromatin to gene function, it is unsurprising that chromatin dysregulation contributes to human disease, including cancer. For example, many proteins that either covalently modify histones or interpret these covalent modifications are implicated in oncogenesis.

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Figure 1: Loss of SNF5 allows misexpression of GLI1 in MRT.

Marina Corral

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Authors and Affiliations

  1. Jeremy F. Reiter is at the Department of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California-San Francisco, San Francisco, California, USA.,

    Jeremy F Reiter

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  1. Jeremy F Reiter
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Correspondence to Jeremy F Reiter.

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Reiter, J. Crippling SWI-SNF makes tumors GLI-ful. Nat Med 16, 1374–1376 (2010). https://doi.org/10.1038/nm1210-1374

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