Abstract
WNT-signaling controls important cellular processes throughout embryonic development and adult life, so any deregulation of this signaling can result in a wide range of pathologies, including cancer. WNT-signaling is classified into two categories: β-catenin-dependent signaling (canonical pathway) and β-catenin-independent signaling (non-canonical pathway), the latter can be further divided into WNT/planar cell polarity (PCP) and calcium pathways. WNT ligands are considered as unique directional growth factors that contribute to both cell proliferation and polarity. Origin of cancer can be diverse and therefore tissue-specific differences can be found in WNT-signaling between cancers, including specific mutations contributing to cancer development. This review focuses on the role of the WNT-signaling pathway in melanoma. The current view on the role of WNT-signaling in cancer immunity as well as a short summary of WNT pathway-related drugs under investigation are also provided.
Highlights
The study of WNT-signaling was initiated in the early 1980 s by the discovery of Wingless, a Drosophila segment polarity gene [1] and the mouse proto-oncogene Int1 [2]
WNT-signaling is divided into two pathways: β-catenin-dependent known as canonical or WNT/β-catenin pathway and β-catenin-independent— termed as non-canonical—which can be further divided into WNT/planar cell polarity (PCP) and calcium pathway that in some circumstances can antagonize WNT/β-catenin-signaling [10]
It has been shown that β-catenin can be a direct partner of SOX10 via protein–protein interactions, which reduces SOX10 protein level in melanoma cells [158]. These results suggest that SOX10 considered as functionally crucial for melanoma survival can be suppressed by WNT/β-catenin-signaling
Summary
The study of WNT-signaling was initiated in the early 1980 s by the discovery of Wingless, a Drosophila segment polarity gene [1] and the mouse proto-oncogene Int1 [2]. The WNT-signaling is evolutionarily conserved and plays an important role in the embryonic development, adult tissue homeostasis and regeneration [4]. It maintains genetic stability and is important for cell fate and differentiation, cell proliferation, cell motility, apoptosis and stem cell maintenance [5]. The β-catenin-dependent pathway mainly controls cell proliferation, whereas β-catenin-independent signaling regulates cell polarity and migration. This distinction, is conventional as these two main pathways form a network with concomitant crosstalk and mutual regulation [11,12]. This review is focused on WNT-signaling in melanoma, a tumor derived from melanocytes that arise from neural crest cells
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