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Bcl-2 inhibits c-fos induction by calcium
X M Qi1, M Simonson, C W Distelhorst
1Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Oncogene
|January 7, 1998
Summary
Bcl-2 protein inhibits calcium signaling pathways that trigger c-fos gene expression. This suggests Bcl-2 plays a role in regulating calcium-dependent gene induction and cell growth.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Cytosolic calcium (Ca2+) transients regulate gene expression involved in cell growth.
- Bcl-2 protein is known to inhibit Ca2+ elevation induced by thapsigargin (TG).
Purpose of the Study:
- To investigate if Bcl-2's modulation of Ca2+ elevation affects calcium signaling.
- To determine Bcl-2's role in the induction of the c-fos gene by TG.
Main Methods:
- Gene expression analysis of c-fos mRNA in response to TG.
- Measurement of c-fos promoter activity using a luciferase reporter assay.
- Manipulation of extracellular Ca2+ to assess the role of Ca2+ signaling.
Main Results:
- TG induced a 20-fold increase in c-fos mRNA in control cells, but only a fivefold increase in Bcl-2 expressing cells.
- Bcl-2 specifically inhibited TG-induced c-fos mRNA elevation, not that induced by phorbol 12-myristate acetate.
- TG-induced c-fos promoter activity was observed in control cells but not in Bcl-2 expressing cells.
- Lowering extracellular Ca2+ prevented TG-induced c-fos expression, confirming the Ca2+ signaling pathway.
Conclusions:
- Bcl-2 regulates Ca2+ signaling pathways.
- Bcl-2 inhibits the induction of c-fos gene expression mediated by Ca2+.
- These findings highlight Bcl-2's role in controlling calcium-dependent cellular responses.