Previous Article | Next Article ![]()
Mol. Cell. Biol., Jan 1996, 211-218, Vol 16, No. 1
GA Preston, TT Lyon, Y Yin, JE Lang, G Solomon, L Annab, DG Srinivasan, DA Alcorta and JC Barrett
The role of c-Fos in apoptosis was examined in two Syrian hamster embryo
cell lines (sup+I and sup-II) and a human colorectal carcinoma cell line
(RKO), using the chimeric Fos-estrogen receptor fusion protein c-FosER. As
previously reported, contrasting responses were observed when these two
cell lines were placed under growth factor deprivation conditions; sup+I
cells were highly susceptible to apoptosis, whereas sup-II cells were
resistant. In this report, we show that the activated c-FosER protein
induces apoptosis in sup-II preneoplastic cells in serum-free medium,
indicating that c-Fos protein can induce apoptotic cell death in these
cells. c-Fos-induced apoptosis was not blocked by the protein synthesis
inhibitor cycloheximide, suggesting that the c-Fos transcriptional
activation activity is not involved. This conclusion was further supported
by the observation that overexpression of v-Fos, which is highly proficient
in transcriptional activation but deficient in the transcriptional
repression activity associated with c-Fos, did not induce apoptosis.
Constitutively expressed Bcl-2 delayed the onset of low-serum-induced
apoptosis in sup+I cells and enhanced survival in sup-II cells. Further,
coexpression of Bcl-2 and c-FosER in sup+I or sup-II cells protected the
cells from c-FosER-induced apoptosis. The possibility that c-FosER- induced
apoptosis requires a p53 function was examined. Colorectal carcinoma
RKOp53+/+ cells, which do not normally undergo apoptosis in serum-free
medium, showed apoptotic DNA fragmentation upon expression and activation
of c-FosER.(ABSTRACT TRUNCATED AT 250 WORDS)
Copyright © 1996, American Society for Microbiology
Induction of apoptosis by c-Fos protein
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»