Effect of triamcinolone acetonide on tyrosinase activity in a human melanoma cell line

• Published in: Cancer research (Chicago, Ill.) Vol. 44; no. 5; pp. 1752 - 1755
• Main Authors: DISORBO, D. M, HARRIS, N. A, NATHANSON, L
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 01.05.1984
• Subjects: Antineoplastic agents; Biological and medical sciences; Carbon Radioisotopes; Catechol Oxidase - metabolism; Cell Cycle - drug effects; Cell Line; DNA Replication - drug effects; General aspects; Humans; Kinetics; Levodopa - metabolism; Medical sciences; Melanoma - enzymology; Monophenol Monooxygenase - metabolism; Pharmacology. Drug treatments; Triamcinolone Acetonide - pharmacology; Tritium; Tyrosine - metabolism; Human; Corticosteroid; Regulation(control); Cell line; Malignant melanoma; Melanogenesis; Α-Tyrosinase; Glucocorticoid; In vitro
• ISSN: 0008-5472; 1538-7445

The synthetic glucocorticoid, triamcinolone acetonide, was found to increase melanogenesis in the human melanoma cell line NEL. Treatment of NEL cells for 24 hr with triamcinolone acetonide (1 X 10(-7) M) increased the activity of the enzyme tyrosinase by 43% and the incorporation of the melanin precursor, L-3,4-dihydroxyphenylalanine, by 23%. Additional studies revealed no change in cyclic AMP levels over an 18-hr test period. A 2-hr preincubation of NEL cells with actinomycin D (10 micrograms/ml) prevented the increase in tyrosinase activity by triamcinolone acetonide. When triamcinolone acetonide was added to a synchronized population of NEL cells, an increase in tyrosinase activity was observed at 16 hr, coinciding with the late S phase of the cell cycle. These results suggest that glucocorticoids are involved in the regulation of melanogenesis in NEL cells by increasing the activity of the rate-controlling enzyme tyrosinase.