Journal
DERMATOLOGY
Volume 213, Issue 3, Pages 192-199Publisher
KARGER
DOI: 10.1159/000095035
Keywords
melanoma; nevus, benign melanocytic; heat shock protein H11
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Funding
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR042647] Funding Source: NIH RePORTER
- NIAMS NIH HHS [AR-42647] Funding Source: Medline
- NIEHS NIH HHS [ES07263] Funding Source: Medline
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Background: The heat shock protein H 11 is silenced in melanoma cell lines, where its forced expression by demethylation with Aza-C triggers apoptosis. Objective: To examine whether H I I is silenced by aberrant DNA methylation in melanoma as compared to nevi and normal skin tissues. Methods: Cell suspensions from benign intradermal nevi, atypical nevi and malignant melanoma tissues were used in reverse-transcriptase PCR and methylation-specific PCR. Paraffin-embedded tissues were stained with HI I antibody. Results: H11 is methylated in 60-75% of melanoma and atypical nevi, but not in normal skin or most benign nevi. Methylation is inversely correlated with H11 expression. Conclusion: The heat shock protein H11 is silenced by aberrant DNA methylation in melanoma, but not benign melanocytic lesions or normal skin melanocytes. The data suggest that H I I is a promising target for the molecular therapy of melanoma. Copyright (c) 2006 S. Karger AG, Basel.
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