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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Relaxin-like ligand-receptor systems are autocrine/paracrine effectors in tumor cells and modulate cancer progression and tissue invasiveness.

Relaxin and INSL3 are novel autocrine/paracrine insulin-like hormones in tumor biology. Both effectors can bind to and activate the leucine-rich G-protein coupled receptors LGR7 relaxin receptor) or LGR8 (relaxin/INSL3 receptor). These relaxin-like ligand-receptor systems modulate cellular functions and activate signaling cascades in a tumor-specific context leading to changes in tumor cell proliferation, altered motility/migration and enhanced production/secretion ofpotent proteolytic enzymes. Matrix-metalloproteinases (MMP), tissue inhibitors of metalloproteinases (TIMP) and acid hydrolases such as cathepsins can facilitate tissue degradation and represent important proteolytic mediators of relaxin-like actions on tumor cell invasion and metastasis. This review presents recent new findings and emphasises the important functions of the relaxin/INSL3 ligand-receptor system as novel autocrine/paracrine effectors influencing tumor progression and tissue invasiveness.[1]

References

  1. Relaxin-like ligand-receptor systems are autocrine/paracrine effectors in tumor cells and modulate cancer progression and tissue invasiveness. Klonisch, T., Bialek, J., Radestock, Y., Hoang-Vu, C., Hombach-Klonisch, S. Adv. Exp. Med. Biol. (2007) [Pubmed]
 
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