c-myc is a proto-oncogene essential for cell growth. When activated, i
ts expression can lead to uncontrolled cell proliferation, transformat
ion and tumorigenesis. The cell line tEMmyc4 is a murine myelomonocyti
c cell line that was established following transformation by v-myc. It
has a high level of v-myc expression and constitutively expresses end
ogenous CSF-1, the monocytic growth and viability factor. Under growth
restricting conditions (high cell density, serum deprivation, heat sh
ock, or dexamethasone addition) cells of this line were found to under
go cell death through apoptosis. The induction of apoptosis by dexamet
hasone was associated with a decrease in constitutive CSF-1 expression
without significant change in v-myc expression. Exogenous CSF-1 rescu
ed these cells from dexamethasone induced-apoptosis. In vivo studies s
howed that tEMmyc4 cells were tumorigenic in syngeneic animals despite
exhibiting some spontaneous apoptosis within the tumour mass. Co-admi
nistration of dexamethasone with the tumour cells significantly inhibi
ted tumor development and the administration of dexamethasone to mice
with established tumors resulted in tumor regression in all mice. This
regression was associated with a high level of apoptosis and necrosis
in the tumors. This study shows a correlation between the in vitro an
d in vivo induction of apoptosis and indicates that cancer cells beari
ng activated oncogenes may be more sensitive to apoptosis induction by
chemotherapeutic agents.