Matrikines, i.e. matrix fragments with
cytokine-like properties, have been ascribed a major role in regulating tumour progression. The invasive front of
melanoma is characterised by intense fragmentation of dermal elastic fibres.
Elastase-mediated elastolysis liberates
elastin fragments, i.e. elastokines, that stimulate several aspects of
melanoma progression such as to enhance
melanoma cell invasion through
type I collagen or increase angiogenesis. Induced-membrane-type 1
metalloprotease (MT1-MMP) expression following
elastin receptor (
S-Gal) occupancy by elastokines is responsible for those
biological activities. Several matrix-derived
peptides with a GXXPG consensus sequence adopting a type VIII beta-turn conformation were as potent as elastokines in promoting angiogenesis in a
Matrigel assay, and
galectin-3 also contains several similar repeats within its N-terminal domain. We propose that
S-Gal might constitute a novel therapeutic target for controlling
melanoma progression.