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Inhibition of growth and squamous‐cell differentiation markers in cultured human head and neck squamous carcinoma cells by β‐all‐trans retinoic acid
Author(s) -
Jetten Anton M.,
Kim Jun S.,
Sacks Peter G.,
Rearick James I.,
Lotan Dafna,
Hong Waun K.,
Lotan Reuben
Publication year - 1990
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910450135
Subject(s) - biology , cell culture , head and neck squamous cell carcinoma , retinoic acid , epidermoid carcinoma , cell growth , cancer research , medicine , cellular differentiation , endocrinology , immunology , microbiology and biotechnology , pathology , carcinoma , cancer , biochemistry , head and neck cancer , gene , genetics
Vitamin A and some of its metabolites such as β‐all‐trans retinoic acid (RA) have been implicated in the regulation of differentiation of normal and malignant epithelial cells in vivo and in vitro. In the present study effects of RA on the growth and differentiation of 7 cell lines derived from human head and neck squamous‐cell carcinomas (HNSCCs) were examined. RA (>0.01 μm) inhibited the proliferation in monolayer culture of 6 of 7 HNSCC cell lines. One cell line (UMSCC‐35) was very sensitive, 5 (UMSCC‐10A, ‐19, ‐30, ‐22B and HNSCC 1483) were moderately sensitive, and I (HNSCC 183) was insensitive. Three of the cell lines (UMSCC‐22B, ‐30, and HNSCC 1483) were capable of forming colonies in semisolid medium—a capability that was suppressed by RA. The HNSCC cell lines expressed various levels of the squamouscell differentiation markers type 1 (particulate, epidermal) transglutaminase (TGase) and cholesterol sulfate (CS). RA treatment (1 μ, 6 days) decreased TGase activity by more than 50% in 3 (UMSCC‐10A, ‐228 and 1483) of the 7 cell lines, and the effect on UMSCC‐22B was dose‐dependent. Type II TGase (soluble, tissue type) activity was detected in 3 cell lines, and after RA treatment its activity increased in HNSCC 1483 and 183 cells and decreased in UMSCC‐19. Following RA treatment, CS levels decreased by 20, 25, 70, 76, 89 and 91% in cell lines UMSCC‐30, ‐10A, 183, UMSCC‐35, ‐22B, and HNSCC 1483, respectively. The suppression by RA of CS accumulation in the 1483 cells was dose‐dependent. Cholesterol sulfotransferase activity, which is responsible for CS synthesis, was suppressed by 40–97% after RA treatment of UMSCC‐19, ‐22B, and HNSCC 1483. Our results demonstrate that RA inhibits the growth and decreases the level of 2 squamous differentiation markers in HNSCC cells.