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Published on: July 17, 2018
CoCl2 induces PC12 cells apoptosis through p53 stability and regulating UNC5B
Minjae Lee1, Hyereen Kang, Sung-Wuk Jang
1Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea.
Brain Research Bulletin
|May 9, 2013
Summary
The receptor uncoordinated 5B (UNC5B) promotes apoptosis under hypoxia. Tumor suppressor p53 regulates UNC5B, influencing cell death pathways and potentially impacting cancer progression.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- The receptor uncoordinated 5B (UNC5B) is known to induce apoptosis without netrin-1.
- The specific role of UNC5B in hypoxia-induced apoptosis remains largely uncharacterized.
Purpose of the Study:
- To elucidate the function of UNC5B in hypoxia-induced apoptosis.
- To investigate the regulatory pathways involved, particularly the p53-dependent pathway in PC12 cells.
Main Methods:
- Characterization of p53-dependent cell death induced by cobalt chloride (CoCl2) in PC12 cells.
- Utilized small interfering RNA (siRNA) to downregulate p53 and UNC5B expression.
- Assessed apoptosis, p53 stabilization, transcriptional activity, p21 expression, and caspase-3 activity.
Main Results:
- CoCl2 treatment increased p53 stabilization and transcriptional activity.
- Downregulation of p53 reduced apoptosis, UNC5B, and p21 expression.
- Ectopic UNC5B enhanced apoptosis, while UNC5B silencing inhibited it.
- Netrin-1 suppressed CoCl2-induced p53 stability, UNC5B expression, and apoptosis.
Conclusions:
- p53 plays a novel role in controlling CoCl2-induced apoptosis by regulating UNC5B.
- UNC5B is a key mediator of hypoxia-induced apoptosis in PC12 cells.
- These findings highlight a new regulatory axis in hypoxia-driven cell death.
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