Abstract
c-Kit, or mast/stem cell growth factor receptor Kit, is a tyrosine kinase receptor structurally analogous to the colony-stimulating factor-1 (CSF-1) and platelet-derived growth factor (PDGF) CSF-1/PDGF receptor Tyr-subfamily. It binds the cytokine KITLG/SCF to regulate cell survival and proliferation, hematopoiesis, stem cell maintenance, gametogenesis, mast cell development, migration and function, and it plays an essential role in melanogenesis. SCF and c-Kit are biologically active as membrane-bound and soluble forms. They can be expressed by tumor cells and cells of the microenvironment playing a crucial role in tumor development, progression, and relapses. To date, few investigations have concerned the role of SCF+/c-Kit+ mast cells in normal, premalignant, and malignant skin lesions that resemble steps of malignant melanoma progression. In this study, by immunolabeling reactions, we demonstrated that in melanoma lesions, SCF and c-Kit were expressed in mast cells and released by themselves, suggesting an autocrine/paracrine loop might be implicated in regulatory mechanisms of neoangiogenesis and tumor progression in human melanoma.
Highlights
Stem cell factor (SCF) is a mast cell growth factor [1] involved in mast cell survival and migration [2]
By immunolabeling reactions, we demonstrated that in melanoma lesions, SCF and c-Kit were expressed in mast cells and released by themselves, suggesting an autocrine/ paracrine loop might be implicated in regulatory mechanisms of neoangiogenesis and tumor progression in human melanoma
One of the main chemoattractant factors released by tumor cells is SCF [2,3,4]. c-Kit (CD 117) is a member of class III transmembrane receptor tyrosine kinases (RTKs), linked to the plateletderived growth factor (PDGF)/colony-stimulating factor-1 (CSF-1) subfamily [5], and acts as a natural receptor of SCF [6]. c-Kit is expressed in mast cells and is involved in their growth and development [7]
Summary
Stem cell factor (SCF) is a mast cell growth factor [1] involved in mast cell survival and migration [2]. Inhibition of the SCF/c-Kit axis inhibits the migration of mouse bone marrow-derived cultured mast cells to tumors in a transplanted tumor model in mice [2], and mutations in c-Kit have been associated with the development of gastrointestinal stromal tumors, various forms of mastocytosis, and mast cell leukaemia [10]. SCF exists as two alternatively spliced variants, the membrane-anchored protein and the soluble one differing in exon 6. Both isoforms are initially membrane-anchored and are composed of an extracellular domain, a transmembrane portion and an intracellular domain, which is not present in
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