Levels of Α‐melanotrophin in the Human Fetal Pituitary Gland Throughout Gestation, in Adult Pituitary Gland and in Human Placenta*

Jf, Wilson

doi:10.1111/j.1365-2265.1982.tb01585.x

Cited by 6 publications

(1 citation statement)

References 35 publications

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“…Some melanoma cells are thus a rich source of immunoreactive a-melanotropin, as can be seen by comparison with the levels detected in POMC-rich tissues from human brain, ranging from 0.70 nmol/g wet tissue in adult pituitary (Wilson, 1982) to 0.90 pmol/g wet tissue in medial nucleus of the thalamus (Arai et al, 1986). However, our results do not allow us to decide whether it is intracellular or can be secreted to the medium.…”

Section: Resultscontrasting

confidence: 56%

Immunoreactive α‐Melanotropin as an Autocrine Effector in Human Melanoma Cells

Loir¹,

Bouchard²,

Morandini³

et al. 1997

European Journal of Biochemistry

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Melanotropin is a peptide having several functions, including the stimulation of melanogenesis and the modulation of proliferation of melanocytes and melanoma cells. It acts through binding to high-affinity receptors of the melanocortin-1 subtype, exclusively expressed in cells of the melanocytic lineage.Elevated levels of immunoreactive a-melanotropin were previously reported in melanoma cell lines, tumours and plasma from patients with melanoma. Here, we show that this high ectopic production of melanotropin is restricted to melanoma and non-pituitary tumours with the same neuroectodermic origin.The occurrence of a melanotropin-specific autocrine loop was further investigated in human melanoma cells. Immunoreactive a-melanotropin was spontaneously released from a melanoma cell line (HBL) expressing melanotropin receptors on the cell surface. This release was significantly increased in the presence of melanotropin-related peptides such as corticotropin-(4-10)-peptide and P-melanotropin, competing for binding to the melanotropin receptor and was directly correlated to the displacement potential of these peptides. Both spontaneous and induced releases of immunoreactive a-melanotropin could be blocked at low temperatures, suggesting the involvement of intracellular protein movement in the release mechanism.The release of immunoreactive a-melanotropin was not significant in melanoma cells expressing very low levels of melanotropin receptors (IGR3) or in non-melanoma cells (SCCI). However, upon expression of the melanocortin-I receptor cDNA into IGR3 cells, spontaneous and competition-induced releases of immunoreactive a-melanotropin were both increased and also blocked at low temperatures. This observation further underlines a role for the melanotropin receptor in the release of immunoreactive a-melanotropin. These experiments indicate that an autocrine loop between the melanocortin-1 receptor and immunoreactive a-melanotropin may be functional in human melanoma cells.

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Section: Resultscontrasting

confidence: 56%