Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.10.3.1 (tyrosinase)
 9,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of prostaglandins (PGs) on the Cloudman S91 melanoma CCL 53.1 cell line indicate that melanogenesis and proliferation are regulated by separate mechanisms that are not necessarily cyclic AMP (cAMP) dependent. These cells responded to PGE1 and PGE2 in a dose-dependent manner, by an increase of tyrosinase activity and by inhibition of proliferation. PGA1 and PGD2 inhibited cellular proliferation and tyrosinase activity, while PGF2 alpha had no effect after 24 h of treatment. PGE1, but not PGE2 or PGD2, increased cellular cAMP levels after 30 min of treatment. Treatment with 10 micrograms/ml PGE1 inhibited cellular proliferation after 4 h and enhanced tyrosinase activity after 12 h. Tyrosinase stimulation by PGE1 required de novo transcription and translation. Actinomycin D, cycloheximide, and the tyrosinase inhibitor phenylthiocarbamide blocked tyrosinase activation but did not alter the inhibitory effect of PGE1 on proliferation. Dibutyryl cAMP and 3-isobutyl-1-methylxanthine augmented tyrosinase activation by PGE1 without enhancing the inhibitory action of PGE1 on cell growth. Neither blockage nor enhancement of the PGE1 effect on tyrosinase altered the PGE1-induced retardation of proliferation. These results are in marked contrast to the traditional concept that elevation of cAMP levels in melanoma cells necessarily results in stimulation of melanogenesis and inhibition of proliferation. The data presented propose independent and possibly alternative pathways for the regulation of these two cellular events.
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PMID:In vitro modulation of proliferation and melanization of S91 melanoma cells by prostaglandins. 243 34

The superpotent and ultraprolonged melanotropic properties of an alpha-melanotropin analog, [Nle4, D-Phe7]-alpha-MSH, were investigated in a Cloudman S91 (CCL 53.1) melanoma cell line. [Nle4, D-Phe7]-alpha-MSH is 100-fold more effective than the native hormone, alpha-melanocyte stimulating hormone (alpha-MSH), in stimulating melanoma cell tyrosinase activity, as determined from their minimum effective doses (10(-11)M and 10(-9)M, respectively). [Nle4, D-Phe7]-alpha-MSH also exhibits a more sustained effect than alpha-MSH on tyrosinase after removal of the melanotropins from the incubation medium. When cells were exposed to alpha-MSH (10(-7)M) for 24 h, residual activity after removal of the hormone was minimally significant. In contrast, under the same experimental conditions [Nle4, D-Phe7]-alpha-MSH treatment induced tyrosinase activity 2-3 fold above basal level, and maintained remarkable stimulatory effects up to 72 h following melanotropin removal. When the exposure time to melanotropins was reduced to 4 h, alpha-MSH failed to elicit significant tyrosinase activity, whereas [Nle4, D-Phe7]-alpha-MSH stimulated significant tyrosinase activity during the first 24 h subsequent to melanotropin removal. Interestingly, this stimulation by the analog increased at 48 h, reached a maximum at 72 h following removal of the melanotropin analog, and remained significantly stimulated for 6 consecutive days in the absence of the analog.
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PMID:[Nle4, D-Phe7]-alpha-MSH: a superpotent melanotropin that "irreversibly" activates melanoma tyrosinase. 300 69

MELANOMA CELLS EXPRESS A PHENOTYPE THAT IS EASY TO RECOGNIZE: the synthesis of melanin. We used this marker to isolate clones of amelanotic variants from large populations of wild-type melanotic clones. Cloudman mouse melanoma (S91, clone M-3, CCL 53.1) was chosen as the parental line because the cells are highly pigmented, grow well as clones in soft agar, and fuse readily with Sendai virus. Subclones (10(7)) of this line were screened without prior mutagenesis, and nine amelanotic variants were isolated. The mutagen ethylmethanesulfonate increased the frequency of variants by three to four orders of magnitude. Wild-type cells had both basal and melanocyte stimulating hormone-inducible tyrosinase activities. The four amelanotic variants that we have examined to date all behaved similarly: they lost basal tyrosinase (EC 1.14.18.1; monophenol monooxygenase) activity but retained melanocyte stimulating hormone-inducible activity; they contained Stage-II melanosomes but no melanized melanosomes; they exhibited growth characteristics similar to those of wild-type cells in culture but produced fewer tumors in mice.
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PMID:Genetic control of melanization: isolation and analysis of amelanotic variants from cultured melanotic melanoma cells. 436 26