Stimulation of the antigen receptor complex leads to transcriptional activation of the c-myc gene in normal human T cells.

Abstract

The expression of the cellular proto-oncogene c-myc has been implicated in growth regulation of both normal and neoplastic cells (for review see Eisenman and Thompson 1986). Quiescent lymphocytes have been shown to express low levels of both c-myc mRNA and protein (Smeland et al. 1987). Stimulation of lymphocytes with mitogens results in the rapid accumulation of c-myc mRNA to levels 10–20 times above background within 2 hours following stimulation (Kelly et al. 1983). Thereafter, c-myc mRNA and protein continue to be expressed throughout the proliferative response of mitogen-activated cells (Hann et al. 1985, Thompson et al. 1985, Rabbitts et al. 1985). The ability of mitogen-activated cells to enter S phase of the cell cycle can be blocked by anti-sense myc oligonucleotides (Heikkila et al. 1987). Constitutive expression of c-myc in murine 3T3 cells has been shown to lead to partial growth factor independence of cell proliferation (Armelin et al. 1984). Finally, agents such as γ-interferon which arrest cell proliferation in vitro are associated with downregulation of c-myc gene expression (Einat et al. 1985). Taken together, these results suggest that the c-myc proto-oncogene may encode a regulatory nuclear protein required for the proliferation of lymphoid cells.