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Steroids inhibit tumor promoting agent induced Epstein‐Barr virus early antigens in raji cells
Author(s) -
Sundar Syam K.,
Ablashi Dharam V.,
Armstrong Gary R.,
Zipkin Mitchell,
Faggioni Alberto,
Levine Paul H.
Publication year - 1981
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.2910280417
Subject(s) - raji cell , proteases , antigen , chemistry , dexamethasone , in vivo , protease , tumor promotion , pharmacology , virus , epstein–barr virus , microbiology and biotechnology , in vitro , biochemistry , medicine , biology , enzyme , immunology , carcinogenesis , gene
Four steroids and one protease inhibitor were evaluated for their effects on 12‐ O ‐tetradecanoyl phorbol 13‐acetate (TPA)‐induced and Epstein‐Barr virus‐induced early antigens (EBV‐EA) in Raji cells. Continuous treatment with dexamethasone, prednisolone, hydrocortisone and cortisone inhibited TPA‐induced EBV‐EA to varying degrees, but the protease inhibitor N ‐α‐ p ‐tosyl L‐lysine chloromethyl ketone‐HCI (TLCK) had no significant effect. None of the agents tested inhibited EBV‐induced EA. In addition, the effect of the steroids was reversible since the removal of these agents resulted in recovery of the percentage of EBV‐EA‐positive cells in TPA‐treated cultures. These results were in agreement with the in vivo experiments of other investigators, who demonstrated inhibition of tumor promotion with steroids. Since TLCK failed to inhibit TPA‐induced EA, it is unlikely that induction of EA by TPA is the result of production of proteases.