Abstract
The incidence of cutaneous melanoma (CM) has increased in the past few decades. The biology of melanoma is characterized by a complex interaction between genetic, environmental and phenotypic factors. A greater understanding of the molecular mechanisms that promote melanoma cell growth and dissemination is crucial to improve diagnosis, prognostication, and treatment of CM. Both small and long non‐coding RNAs (lncRNAs) have been identified to play a role in melanoma biology; microRNA and lncRNA expression is altered in transformed melanocytes and this in turn has functional effects on cell proliferation, apoptosis, invasion, metastasis, and immune response. Moreover, specific dysregulated ncRNAs were shown to have a diagnostic or prognostic role in melanoma and to drive the establishment of drug resistance. Here, we review the current literature on small and lncRNAs with a role in melanoma, with the aim of putting into some order this complex jigsaw puzzle.
Highlights
The incidence of cutaneous melanoma (CM) has increased in the past few decades
A greater understanding of the molecular mechanisms that promote melanoma cell growth and dissemination is crucial to improve diagnosis, prognostication, and treatment of CM. Both small and long non-coding RNAs have been identified to play a role in melanoma biology; microRNA and lncRNA expression is altered in transformed melanocytes and this in turn has functional effects on cell proliferation, apoptosis, invasion, metastasis, and immune response
Cutaneous melanoma typically arises on sun-exposed skin because of the progressive accumulation of UV radiation-induced genetic alterations
Summary
The incidence of cutaneous melanoma (CM) has increased in the past few decades. The worldwide highest incidence is reported in Australia (36–50/100 000 people). BRAF gene mutations are found in 52% of melanomas (Cancer Genome Atlas Network, 2015), and 90% of those mutations are a single nucleotide alteration (nucleotide 1799 T>A), resulting in substitution of glutamic acid for valine (BRAFV600E) (Ascierto et al, 2012). This mutation causes the constitutive activation of the kinase and insensitivity to negative feedback mechanisms, promoting angiogenesis (via HIFa and VEGF activation), apoptosis evasion, invasion and metastasis (Maurer et al, 2011). This could be avoided by targeting other players in the tumor microenvironment or acting on other dysregulated molecules inside the tumor cell, including non-coding RNAs (ncRNAs)
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