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ShareMay 11, 2010 — Dr. Victor Tron and colleagues of Queen's University, Kingston, Ontario, Canada have identified differential expression of miRNAs as a contributing factor in melanoma development. These results are presented in the May 2010 issue of The American Journal of Pathology.
Melanoma, a malignant tumor of melanin-producing cells in the skin, is one of the least common forms of skin cancer, but causes most (75%) of skin cancer-related deaths. miRNAs are a class of small genetic molecules that, instead of coding for genes, regulate gene expression and thus may play a role in cancer development.
To examine the hypothesis that differential expression of miRNAs may contribute to melanoma development, Chen et al compared levels of miRNA expression between benign lesions and metastatic melanoma. Of the miRNAs examined, 31 were expressed differently between benign and cancerous lesions, with one, miR-193b, significantly decreased in all melanoma tissues examined. High levels of miR-193b expression in tumor cells inhibited proliferation as well as downregulated numerous genes, including a gene that regulates cell division. These results suggest that miR-193b dysregulation may contribute to melanoma development by altering cell proliferation.
Dr. Tron's group suggests that "further study of miR-193b in primary melanomas is necessary to understand whether downregulation of miR-193b is an early event in melanoma progression. Because miR-193b appears to have anti-proliferative effects in melanoma cells, it may have potential as a novel therapeutic agent for melanoma treatment. "
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The above story is reprinted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.
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Journal Reference:
- Chen J, Feilotter HE, Paré GC, Zhang X, Pemberton JGW, Garady C, Lai D, Yang X, Tron VA. MicroRNA-193b Represses Cell Proliferation and Regulates Cyclin D1 in Melanoma. American Journal Of Pathology, 2010; 176 (5): 2520 DOI: 10.2353/ajpath.2010.091061
Note: If no author is given, the source is cited instead.
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