Metastasis suppressor protein. May regulate events downstream of cell-matrix adhesion, perhaps involving cytoskeletal reorganization. Generates a C-terminally amidated peptide, metastin which functions as the endogenous ligand of the G-protein coupled receptor GPR54. The receptor is also essential for normal gonadotropin-released hormone physiology and for puberty. The hypothalamic KiSS1/GPR54 system is a pivotal factor in central regulation of the gonadotropic axis at puberty and in adulthood. Intracerebroventricular administration induces an increase in serum LH and FSH levels in prepubertal male and female as well as in adult animals. Highest levels in the cecum and colon. Moderate levels present in the liver, spleen, kidney, ovary, uterus and small intestine. Low levels in the stomach, pancreas and placenta. Expressed only moderately in the placenta. Persistent expression is detected in hypothalamus throughout postnatal development, with maximum expression levels at puberty in both male and female. Hypothalamic expression is sensitive to neonatal imprinting by estrogen. Expression is higher in the hypothalamus than in the brainstem and spinal cord. In the brain, metastin-like immunoreactivity is found mainly in three groups of cells: dorsomedial hypothalamic nucleus, nucleus of the solitary tract, and caudal ventrolateral medulla. Expression observed in trophoblast giant cells (TGCs), the placenta-derived cell lineage aligned at the boundary between the uterus and placenta, at embryonic days 12.5 (E12.5). Expressions gradually decreased during placental maturation, and the signal is no more detectable in the cells at E18.5. Belongs to the KISS1 family.