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CREB-mediated Bcl-2 expression in trichosanthin-induced Hela cell apoptosis
Ping Wang1, Hui Yan, Ji-Cheng Li
1Institute of Cell Biology, Zhejiang University, Hangzhou 310058, PR China.
Trichosanthin (TCS) induces Hela cell apoptosis by decreasing Bcl-2 and phosphorylated cyclic AMP response element-binding protein (CREB). CREB activation is critical for regulating Bcl-2 expression during TCS-induced cell death.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Bcl-2 is crucial for regulating cell death.
- Bcl-2 expression is modulated by the transcription factor cyclic AMP response element-binding protein (CREB).
- Trichosanthin (TCS) treatment leads to down-regulation of Bcl-2 during apoptosis.
Purpose of the Study:
- To investigate the role of CREB activation in trichosanthin (TCS)-induced apoptosis in Hela cells.
- To elucidate the regulatory mechanism of Bcl-2 expression in TCS-mediated cell death.
Main Methods:
- Assessing protein levels of Bcl-2 and phosphorylated CREB in Hela cells treated with TCS.
- Utilizing cAMP agonists to counteract TCS effects.
- Employing antisense treatment to suppress CREB expression.
- Using a CRE decoy oligonucleotide to block CREB-binding protein interaction with the Bcl-2 CRE.
Main Results:
- TCS-induced Hela cell apoptosis correlated with decreased Bcl-2 and phosphorylated CREB levels.
- Combined treatment with TCS and cAMP agonists abolished the inhibitory effect on Bcl-2 and CREB.
- Suppression of CREB expression or blocking CREB-binding protein interaction abrogated TCS-mediated Bcl-2 down-regulation.
Conclusions:
- CREB plays a critical role in regulating Bcl-2 expression during TCS-induced Hela cell apoptosis.
- The findings highlight a signaling pathway involving CREB in the control of cell death mediated by TCS.
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