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Inhibition of human oral squamous carcinoma cell (SCC‐25) proliferation by prostaglandin E 2 and vitamin E succinate
Author(s) -
ElAttar T. M. A.,
Lin H. S.
Publication year - 1993
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1993.tb00135.x
Subject(s) - prostaglandin e2 , cell growth , prostaglandin , dna synthesis , prostaglandin e , vitamin e , in vitro , in vivo , endocrinology , stimulation , medicine , vitamin , cell culture , thymidine , cell , biochemistry , chemistry , biology , antioxidant , genetics , microbiology and biotechnology
The primary objective of this investigation was to study the effect of D‐alpha‐tocopherol acid succinate (vitamin E succinate) and prostaglandin E 2 (PGE 2 ), individually and in combination, on the proliferation of human tongue squamous carcinoma cells (SCC‐25) in vitro. Test compounds in varying concentrations were incubated with cells in serum‐free Dulbecco's Modified Eagle's Medium‐Ham's F‐12 Medium (50:50), supplemented with 0.1% albumin for sixteen hours. Cell proliferation was measured by the incorporation of [3H] thymidine in acid‐insoluble material (i.e. DNA). Prostaglandin E 2 and vitamin E succinate, individually at 10 −9 10 −6 M, caused significant dose‐dependent inhibition in DNA synthesis. A combined dose of each compound at 10 −5 M resulted in significant additive inhibition which averaged 43.53% (p < 0.005). Addition of indomethacin (INDO) to cell cultures induced significant dose‐dependent stimulation in DNA synthesis. Hence, we might suggest that the overall potential of vitamin E in controlling malignant cell proliferation in vivo could be due to its own effect combined with that of endogenous PGs which are normally produced in excessive amounts by malignant cells.