C-myc promotes survival of WEHI 231 B lymphoma cells from apoptosis.

Abstract

The c-myc oncogene has been implicated in control of cell proliferation, differentiation, as well as neoplastic transformation. More recently, overexpression or inappropriate time of expression of the c-myc gene has been found to promote apoptosis. Cleveland and coworkers observed that addition of a vector expressing c-Myc protein accelerated apoptosis following IL-3 deprivation of the 32D Independent myeloid cell line [3]. Similarly Evan and coworkers [10] found that transfection of 3T3 fibroblast cells with c-myc expression vectors led to enhanced levels of apoptosis upon growth arrest either by serum or isoleucine deprivation, or a thymidine block. These findings have been further extended using c-myc antisense oligonucleotides. Green and coworkers have shown that addition of these oligonucleotides to immature T cells and some T cell hybridomas, inhibited c-myc expression and prevented T cell receptor mediated apoptosis [23]. Together these results strongly suggest that inappropriate overexpression of c-myc promotes apoptosis in some cell systems.