Abstract |
The Ca(2+) - binding protein recoverin is normally specific for the retina. Recoverin aberrantly expressed in lung and melanoma tumors can trigger the host immune response followed by the development of a paraneoplastic neurological syndrome represented by cancer- and melanoma-associated retinopathy, respectively. The mechanisms, underlying the aberrant expression of recoverin in tumor cells, have remained unknown. The data obtained in this study suggest that (i) DNA methylation participates in the repression of synthesis of mRNA for recoverin in normal tissues and (ii) aberrant hypomethylation of the recoverin gene region, overlapping the promoter up-stream of the first exon and the first exon itself, is involved in the aberrant expression of recoverin in tumor cells.
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Authors | Alexandr V Bazhin, Charles De Smet, Marina O Golovastova, Jan Schmidt, Pavel P Philippov |
Journal | Experimental dermatology
(Exp Dermatol)
Vol. 19
Issue 11
Pg. 1023-5
(Nov 2010)
ISSN: 1600-0625 [Electronic] Denmark |
PMID | 20812967
(Publication Type: Letter)
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Copyright | © 2010 John Wiley & Sons A/S. |
Chemical References |
- Recoverin
- Decitabine
- DNA Modification Methylases
- Azacitidine
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Topics |
- Azacitidine
(analogs & derivatives, pharmacokinetics, pharmacology)
- Cell Line, Tumor
- DNA Methylation
(drug effects, genetics)
- DNA Modification Methylases
(antagonists & inhibitors)
- Decitabine
- Exons
(genetics)
- Gene Expression Regulation, Neoplastic
- Humans
- Lung
(metabolism)
- Melanoma
(metabolism)
- Neoplasms
(genetics, metabolism, pathology)
- Promoter Regions, Genetic
(genetics)
- Recoverin
(genetics)
- Skin
(metabolism)
- Small Cell Lung Carcinoma
(metabolism)
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