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Adv Exp Med Biol. 2007;612:104-18.

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

Author information

1
Department of Human Anatomy and Cell Science, Faculty of Medicine, University of Manitoba, 130 Basic Medical Science Bldg., 730 William Avenue, Winnipeg, Manitoba, Canada R3E 0W3. klonisch@cc.umanitoba.ca

Abstract

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.

PMID:
18161484
DOI:
10.1007/978-0-387-74672-2_8
[Indexed for MEDLINE]

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