Premium
Relationship of cellular oncogene expression to inhibition of growth and induction of differentiation of Daudi cells by interferons or TPA
Author(s) -
Clemens Michael J.,
Tilleray Vivienne J.,
James Robert,
Gewert Dirk R.
Publication year - 1988
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240380404
Subject(s) - interferon , cell growth , microbiology and biotechnology , oncogene , cellular differentiation , gene expression , biology , alpha interferon , cell culture , growth inhibition , cell , dna synthesis , cancer research , chemistry , gene , dna , immunology , cell cycle , biochemistry , genetics
Human α or β interferons inhibit the proliferation of Daudi Burkitt lymphoma cells and induce the differentiation of these cells towards a mature plasma cell phenotype. Similar responses are seen when Daudi cells are treated with the phorbol ester, TPA. Both interferons and TPA down‐regulate expression of the c‐myc oncogene in these cells. Although TPA can mimic the effect of interferon on cell differentiation, it does not induce 2′5′ oligoadenylate synthetase or the interferon‐sensitive mRNAs, 6–16 or 9–27. Thus chronic stimulation of protein kinase C by TPA cannot mimic all of the effects of interferon treatment on gene expression. Inhibition of ADP‐ribosyl transferase activity by 3‐methoxybenzamide impairs interferon‐ or TPA‐induced differentiation of Daudi cells. This agent induces a higher level of c‐myc mRNA in the cells and stimulates the incorporation of [ 3 H]thymidine into DNA; although these effects are partially counteracted by interferon or TPA treatment, the elevated expression of the c‐myc gene may be sufficient to prevent terminal differentiation and allow cell proliferation to continue.