Acetylation of the Proto-Oncogene EVI1 Abrogates Bcl-xL Promoter Binding and Induces Apoptosis Regulation of Bcl-xL by EVI1
2011
EVI1 Regulates Bcl-xL and Apoptosis in Cancer Cells
publication
10 minutes
Evidence: moderate
Author Information
Author(s): Anjan Kumar Pradhan, Alok Das Mohapatra, Kasturi Bala Nayak, Soumen Chakraborty
Primary Institution: Institute of Life Sciences, Bhubaneswar, Orissa, India
Hypothesis
EVI1 directly induces the expression of Bcl-xL and inhibits apoptosis.
Conclusion
EVI1 binds to the Bcl-xL promoter and regulates its expression, affecting apoptosis in cancer cells.
Supporting Evidence
- EVI1 directly binds to the Bcl-xL promoter and activates its transcription.
- Acetylation of EVI1 reduces its ability to bind to the Bcl-xL promoter.
- EVI1 positive samples showed higher Bcl-xL expression compared to EVI1 negative samples.
- Downregulation of EVI1 leads to decreased Bcl-xL expression.
Takeaway
EVI1 is a protein that helps cancer cells survive by stopping them from dying, and it does this by turning on another protein called Bcl-xL.
Methodology
The study used ChIP analysis, real-time PCR, and luciferase assays to investigate the interaction between EVI1 and the Bcl-xL promoter.
Statistical Information
P-Value
0.0141
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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