Release date: 2016-03-25
In collaboration with researchers at the University of Ghent in Belgium, scientists from VIB/Louven University have uncovered an unusual link between malignant melanoma and the non-coding RNA gene SAMMSON. The SAMMSON gene is specifically expressed in human malignant melanoma, and it is striking that the growth of invasive skin cancer is highly dependent on this gene. The findings may pave the way for improved diagnostic tools and treatment for skin cancer.
The study, led by VIB/Leuven University's Jean-Christophe Marine and the University of Ghent, Professor Pieter Mestdagh, is expected to cause quite a stir, and the relevant research paper is published in the top science journal Nature.
Because it does not contribute to protein coding, a large part of the human genome has long been regarded as "junk DNA", but recent studies have shown that these so-called "junk DNA" do generate some basic biological processes and diseases. Many non-coding RNAs that play an important role. For several years, Professor Marine and Professor Mestdagh's laboratory have been studying the contribution of non-coding RNA genes to cancer. They are especially interested in long-chain non-coding RNA (lncRNA) genes.
Screening lncRNA gene in cancer
To assess the importance of specific long-chain non-coding RNA genes in the development of skin cancer, VIB Laboratories worked with the Department of Pediatrics and Medical Genetics at Ghent University. The Ghent University research team led by Pieter Mestdagh completed a large-scale screening study of the expression of many lncRNAs between different cancer types. The screening found that SAMMSON is a melanoma-specific lncRNA.
Pieter Mestdagh said: "Our research confirms that the long-chain non-coding RNA gene SAMMSON is specifically expressed in human melanoma, which replicates or expands in approximately 10% of cases. Also, in normal melanocytes and all other normal SAMMSON is not found in adult tissues. The unique expression profile of SAMMSON leads us to speculate that this gene may play an important role in the pathogenesis of melanoma."
The VIB team confirmed that SAMMSON is specifically expressed in more than 90% of human malignant (rather than benign) melanoma clinical samples. In addition, they confirmed that the SAMMSON gene was activated by the melanoma-specific transcription factor SOX10, thereby explaining its melanoma-specific expression pattern.
Melanoma is addictive to SAMMSON
Moreover, VIB scientists found that melanoma cells are significantly dependent on the expression of SAMMSON. When reducing SAMMSON in melanoma cultures, cancer cells quickly die in large numbers, regardless of the type of melanoma. This led to the key conclusion of “SAMMSON addictionâ€, which is reflected in the title of the paper “Melanoma addiction to the lineage-restricted lncRNA gene SAMMSONâ€.
Jean-Christophe Marine said: "In vitro and in preclinical studies in mice, we demonstrated that blocking SAMMSON by targeted antisense molecules significantly reduced melanoma growth. Importantly, we also found that SAMMSON was recruited. To the mitochondria, the organelle that supplies energy to cancer cells. By promoting SAMMSON degradation, these antisense molecules disrupt important mitochondrial activity and prevent tumor growth. In other words: SAMMSON addiction is something we can combat by targeted therapy. An obvious vulnerability and does not affect the normal cells of the host or patient."
Next clinical trial
Further research is necessary to firmly establish the hypothesis of this study: SAMMSON can be used as a biomarker for malignant melanoma. Because the SAMSSON gene is not expressed in benign melanoma, its emergence may be a key factor in the development of new diagnostic tools that significantly improve the prognosis of melanoma.
Perhaps more importantly, the findings laid a solid foundation for the development of new treatments for skin cancer. The same research team will soon start toxicology research, and now it is in talks with different industrial companies to explore future mutually beneficial cooperation.
Source: Biopass
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