Hormonal Regulation of Melanogenesis in Mouse Melanoma and in Human Melanocytes

Activation of melanogenesis by vacuolar type H+‐ATPase inhibitors in amelanotic, tyrosinase positive human and mouse melanoma cells

“…A number of studies have suggested that tyrosinase in pigment cells does not necessarily exist in a catalytically optimal state [6,32]. There have also been several reports that activation of this enzyme can occur independently of increases in its synthesis [5,33].…”

“…Recently, there has been interest in the role of post-translational events in the regulation of tyrosinase activity [2^5]. It is recognised that variations in tyrosinase activity in di¡erent pigment cells cannot be explained on the basis of enzyme abundance [6]. For instance, amelanotic and pigmented subclones of melanoma cells can have similar levels of tyrosinase protein [7] and the same has been reported for melanocytes from light Caucasian and black skin [8].…”

Bicyclic Monoterpene Diols Induce Differentiation of S91 Melanoma and PC 12 Pheochromocytoma Cells by a Cyclic Guanosine‐Monophosphate‐Dependent Pathway

“…In clinical trials, MSH analogues stimulated melanogenesis in human skin, but they required injection, and tanning was most pronounced in areas previously tanned (Levine et al, 1991). 3-Isobutyl-l-methylxanthine (IBMX) and diacylglycerol (DAG) demonstrated efficacy in cell culture and animal studies (Allan et al, 1995;Fuller et al, 1993;Fuller, 19981, but there are no published reports regarding human trials. Although IBMX and DAG stimulate melanogenesis via the protein kinase (PK) A and PKC intracellular signaling pathways, respectively, UV radiation does not appear to stimulate melanogenesis by either of these pathways (Carsberg et al, 1994;Friedmann and Gilchrest, 1987;Romero-Graillet et al, 1996).…”

Melanocortin Receptors: Identification and Characterization by Melanotropic Peptide Agonists and Antagonists

“…Recent results clearly document functional melanotropin receptors as membrane components of NHEMs (Suzuki et al, 1996). Several recent publications document the actions of melanotropins on NHEMs (Abdel-Malek et al, 1994;Fuller et al, 1993;Graeven and Herlyn, 1992;Herlyn et al, 1988;Hunt et al, 1994;Hunt, 1995;Mancianti et al, 1993). To determine the functionality of NHEM MCRs, we incubated the cells continuously in the presence or absence of [Nle4,DPhe7]a-MSH (10'7M) for 110 days.…”

“…a-MSH elicits its effects by binding to membrane MCRs, an event that results in stimulation of adenylate cyclase activity and in an increase in intracellular CAMP levels within 20 min. An increase in tyrosinase activity commences after 6-8 hr of continuous exposure to a-MSH, and involves both transcriptional and translational events since the response is blocked by either actinomycin D or cycloheximide (Fuller et al, 1993). After exposure of S-91 melanoma cells to [Nle4,DPhe7]a-MSH for only 4 hr or less, genomic mechanisms involving both messenger RNA synthesis and protein synthesis are turned on for at least six days subsequent to removal of the hormone analog, and in spite of continued cell division (Hadley et al, 1985).…”