Laure Aurelian

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The Levels of H11/HspB8 DNA methylation in human melanoma tissues and xenografts are a critical molecular marker for 5-Aza-2'-deoxycytidine therapy.

Cynthia C Smith; Baiquan Li; Juan Liu; Kie-Sok Lee; Laure Aurelian (Profiled Author: Laure Aurelian)

Department of Pharmacology and Experimental Therapeutics, School of Medicine, University of Maryland, Baltimore, USA.
Cancer investigation 2011;29(6):383-95.

H11/HspB8 is a functionally distinct small heat shock protein. It causes growth arrest in melanocytes, associated with the inhibition of Cyclin E/Cdk2 and β-catenin phosphorylation at the transcriptional activity site Ser(552) and is silenced through DNA methylation in 27/35 (77%) melanoma tissues/early cultures. 5-Aza-2'-deoxycytidine (Aza-C) induces melanoma cell death correlated with the levels of H11/HspB8 DNA methylation (p < .001). In line with low/moderate H11/HspB8 methylation, PI3-K inhibition increases Aza-C-induced cell death. Aza-C inhibits the growth of melanoma xenografts related to the levels of H11/HspB8 methylation, and a nonmethylated/non-TAK1 binding H11/HspB8 mutant confers Aza-C resistance. H11/HspB8 is a potential molecular marker for demethylation therapies.

1 Originating Grant

• 1.

  AURELIAN, LAURE

  Apoptosis of skin melanoma by the new Hsp H11

  9 August 2007 - 30 June 2012

  NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES

Scientific Context

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