Abstract
Simple SummaryLong non-coding RNAs (lncRNAs) are heterogeneous RNA molecules that can regulate a plethora of cellular processes including proliferation, differentiation, migration, invasion and apoptosis through diverse mechanisms. Growing evidence indicates that aberrant expression of lncRNA leads to the development and progression of cancer, including melanoma, and might contribute to the acquisition of drug resistance. Moreover, their tightly-regulated expression and their high tissue and disease specificity make them promising biomarkers in non-invasive diagnostics of cancer. This review summarizes current knowledge regarding the involvement of lncRNAs in melanoma along with their possible use as diagnostic biomarkers.Melanoma is the most lethal skin cancer, with increasing incidence worldwide. The molecular events that drive melanoma development and progression have been extensively studied, resulting in significant improvements in diagnostics and therapeutic approaches. However, a high drug resistance to targeted therapies and adverse effects of immunotherapies are still a major challenge in melanoma treatment. Therefore, the elucidation of molecular mechanisms of melanomagenesis and cancer response to treatment is of great importance. Recently, many studies have revealed the close association of long noncoding RNAs (lncRNAs) with the development of many cancers, including melanoma. These RNA molecules are able to regulate a plethora of crucial cellular processes including proliferation, differentiation, migration, invasion and apoptosis through diverse mechanisms, and even slight dysregulation of their expression may lead to tumorigenesis. lncRNAs are able to bind to protein complexes, DNA and RNAs, affecting their stability, activity, and localization. They can also regulate gene expression in the nucleus. Several functions of lncRNAs are context-dependent. This review summarizes current knowledge regarding the involvement of lncRNAs in melanoma. Their possible role as prognostic markers of melanoma response to treatment and in resistance to therapy is also discussed
Highlights
Melanoma is the most lethal form of melanocyte-originated skin cancer and its incidence continues to increase worldwide [1,2]
Survival-Associated Mitochondrial Melanoma Specific Oncogenic Non-Coding RNA (SAMMSON) is a melanoma-specific long noncoding RNAs (lncRNAs) and its expression is positively regulated by SRY-box transcription factor 10 (SOX10), a transcription factor responsible for the development of neural and pigment cells, that derive from the neural crest
Despite recent advances in treatment and development of inhibitors that selectively target mutated BRAF and other elements of the MAPK pathway in melanoma, or inhibitors of immune checkpoints PD-1 and CTLA-4, low response rate or acquired resistance to these drugs remain the main cause of melanoma recurrence and patient deaths
Summary
Melanoma is the most lethal form of melanocyte-originated skin cancer and its incidence continues to increase worldwide [1,2]. The members of miR-200 family are well-known tumor suppressors that modulate cell proliferation, migration, invasion and drug resistance in various cancers, including melanoma [73] Another lncRNA that represses miR-200 family expression through EZH2-mediated binding to miR-200 promoter is plasmacytoma variant translocation 1 (PVT1), upregulated in melanoma. Survival-Associated Mitochondrial Melanoma Specific Oncogenic Non-Coding RNA (SAMMSON) is a melanoma-specific lncRNA and its expression is positively regulated by SOX10, a transcription factor responsible for the development of neural and pigment cells, that derive from the neural crest. Increased expression of TTN-AS1 results in significant upregulation of TTN at mRNA and protein levels, and high expression of both genes induces melanoma cell proliferation, suppresses cell apoptosis, promotes cell migration in vitro and tumor growth and metastasis in vivo. Cmuloelsec(ulnlecsR(NlnAcRs NanAds acnirdcRciNrcARsN) Aasre) aarcetaivcetilvyeliynvinovlvoeldvedininmmelealnaonmomagaegneenseissi,s,aanndd tthheeiirr ssppoonnggiinnggaaccttiivviittyyiissssuummmmaarriizzeeddiinnTTable 2
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