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Updated: Aug 14, 2026
07:42
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
Induction of apoptosis by c-Fos protein
1Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
Molecular and Cellular Biology
|January 1, 1996
Summary
The c-Fos protein can trigger apoptosis, a form of programmed cell death, in a p53-dependent manner. This process does not require new protein synthesis and is inhibited by Bcl-2 protein, offering insights into cancer cell death regulation.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- The role of c-Fos in programmed cell death (apoptosis) is complex and cell-type dependent.
- Previous studies showed differential apoptosis susceptibility in Syrian hamster embryo cell lines (sup+I and sup-II) under growth factor deprivation.
Purpose of the Study:
- To investigate the role of c-Fos protein in inducing apoptosis.
- To determine the involvement of transcriptional activity and p53 in c-Fos-mediated apoptosis.
- To examine the interaction between c-Fos, Bcl-2, and p53 in apoptosis regulation.
Main Methods:
- Utilized a chimeric Fos-estrogen receptor fusion protein (c-FosER) to activate c-Fos.
- Employed Syrian hamster embryo cell lines (sup+I, sup-II) and human colorectal carcinoma RKO cells (p53+/+ and p53-deficient).
- Assessed apoptosis induction, DNA fragmentation, and protein synthesis inhibition (cycloheximide).
- Investigated the effect of Bcl-2 overexpression and v-Fos expression.
Main Results:
- Activated c-FosER induced apoptosis in resistant sup-II cells, independent of protein synthesis.
- Overexpression of v-Fos, proficient in transcriptional activation, did not induce apoptosis.
- Bcl-2 expression delayed apoptosis in sup+I cells and protected both cell types from c-FosER-induced apoptosis.
- c-FosER induced apoptosis in RKO cells, and this effect was blocked when p53 was diminished.
Conclusions:
- c-Fos protein plays a direct role in inducing apoptosis.
- c-Fos-mediated apoptosis is p53-dependent and does not require new protein synthesis.
- Bcl-2 protein can inhibit c-Fos-induced apoptosis, suggesting a regulatory mechanism involving these proteins.
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