Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

D-alpha tocopheryl succinate (vitamin E succinate), which is known to induce differentiation and growth inhibition in murine B-16 melanoma cells, reduced basal and melanocyte-stimulating hormone (MSH)-stimulated adenylate cyclase (AC) activity in vitro. Vitamin E succinate treatment also reduced sodium fluoride- and forskoline-stimulated AC activity of melanoma cells in vitro. Treatment of cells with vitamin E succinate (6 micrograms/ml] for a period of 24 hours was sufficient to reduce MSH-stimulated AC activity. Other forms of vitamin E, such as d1-alpha tocopheryl nicotinate, d1-alpha tocopheryl acetate, and d1-alpha tocopherol, which did not affect growth or morphology of melanoma cells, were relatively less effective in altering basal and MSH-stimulated AC activity. Retinoic acid, which inhibited the growth of B-16 melanoma cells, also reduced basal and MSH-, NaF-, and forskolin-stimulated AC activity in vitro. Prostaglandin A2, which inhibited growth and altered morphology, did not change basal or MSH-stimulated AC activity. These results show that one of the mechanisms of action of vitamin E succinate and retinoic acid on melanoma cells may involve reduction of basal and MSH-sensitive AC activity, and this vitamin effect is not necessarily related to growth inhibition.
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PMID:Alpha tocopheryl succinate inhibits melanocyte-stimulating hormone (MSH)-sensitive adenylate cyclase activity in melanoma cells. 369 13

The direct effect of continuous exposure to prostaglandins on the cloning efficiency and proliferative capacity of human malignant melanoma colony-forming cells in soft agar was evaluated. Prostaglandin A1 (PGA1) and prostaglandin E1 (PGE1) effected a dose-dependent inhibition of colony formation and proliferative capacity. PGA1 at a concentration of 5 microgram/ml reduced colony formation of cells from human melanoma cell strains C8054, C8130, and C822 by at least 85%. PGA1 also inhibited colony formation of cells obtained directly from biopsies of melanoma tissues from eight patients by greater than 70% at a concentration of 5 microgram/ml. A steep dose-response curve was evident by the little effect of PGA1 on colony formation at a concentration of 0.5 microgram/ml. The mean 50% inhibitory doses for PGA1 and PGE1 were 1.25 and 4.25 microgram/ml, respectively. Prostaglandin A2 was much less effective than PGA1 in inhibiting melanoma colony formation. The related prostaglandins (prostaglandin B1, prostaglandin F1 alpha, and prostaglandin E2 alpha) had little or no effect on colony formation. Overall, these results suggested that the presence of a carbonyl group at position 9 of the cyclopentane ring may be required for inhibitory activity as prostaglandins of the A and E series inhibited human melanoma cell growth. PGA1 and PGE1 did not effect a rise in cyclic adenosine 3':5'-monophosphate levels in C8054 and C8130 cells. However, while alpha-melanocyte-stimulating hormone and prostaglandin F2 alpha did generate a rise in adenosine 3':5'-monophosphate levels in C8054 cells, these hormones had no effect on colony formation. These results are consistent with the notion that the PGA1 and PGE1 inhibition of melanoma colony-forming cells occurs via a noncyclic nucleotide mechanism.
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PMID:Inhibition of human malignant melanoma colony-forming cells in vitro by prostaglandin A1. 657 55