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Ramirez, M.T, Chow, A., Hirschhorn, C.D., Terwey, T.H., Hochma, A.A., Lu, S., Miles, R.C., Sakaguchi, S., Houghton, A.N. and Van den Brink, M.R. (2006) Glucocorticopid-induced TNF receptor family related gene activation overcomes tolerance/ignorance to melanoma differentiation antigens and enhances antitumor immunity. Journal of Immunology, 176(11), 6434-6442.

has been cited by the following article:

• TITLE: Potential mechanism for the effects of dexamethasone on growth of human melanoma cells in vitro

  AUTHORS: Abdel-Moneim M. Osman, Omimah A. Nasseir, Naglaa R. Ismail

  KEYWORDS: Melanoma Cells; Dexamethasone; Glucocorticoid Receptors

  JOURNAL NAME: Health, Vol.2 No.8, August 25, 2010

  ABSTRACT: This study deals with the inhibitory effects of dexamethsone on the proliferation of a human melanoma cell line in vitro. A retarded cell proliferation was observed in M-5A cells with the presence of specific high affinity glucocorticoid steroid receptors. There was a correlation between the number of glucococrticoid binding sites and the reduction of cell proliferation in term of reduced plating efficiency. Arrest or accumula- tion of M-5A cells in G1 phase or both in G1 and G2 phase appeared to be involved in the growth inhibitory effect by dexamethsone. The magnitude and duration of cell cycle arrest up to 72 hours were dose dependent. There was a correlation between the duration of the disturbance of the cell cycle progression in M-5A cells after dexamethsone treatment and the inhibition of cell proliferation. Synthesis of receptor protein was not specifically stimulated or inhibited relative to the effect on cellular protein content in general. This may conclude that in the melanoma M-5A cell, death after glucocorticoid treatment is somehow related to the glucocorticoid receptor content and to the disturbance of cell cycle distribution.