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Zinc induces mitochondria apoptogenesis in prostate cells
1Cellular and Molecular Biology Section, Department of Oral and Craniofacial Biological Sciences, University of Maryland Dental School, Baltimore, Maryland 21201, USA. pfeng@umaryland.edu
Molecular Urology
|June 14, 2000
Summary
High intracellular zinc levels in prostate cells trigger programmed cell death (apoptosis) via the mitochondria. This discovery reveals a new mechanism for zinc in regulating prostate cell growth.
Area of Science:
- Cell Biology
- Biochemistry
- Oncology
Background:
- Prostate secretory epithelial cells uniquely accumulate high intracellular zinc levels.
- Zinc accumulation inhibits prostate cell growth, partly by increasing apoptosis.
- The role of mitochondrial pathways in zinc-induced apoptosis was investigated.
Purpose of the Study:
- To determine if zinc-induced apoptosis in prostate cells involves mitochondrial apoptogenesis.
- To elucidate the mechanism of zinc's effect on prostate cell growth regulation.
Main Methods:
- PC-3 human malignant prostate cells (zinc-accumulating) were treated with physiologic zinc levels.
- Rat ventral prostate cells (zinc-accumulating) and PZ-HPV-7 human prostate cells (non-zinc-accumulating) were also studied.
- Mitochondrial cytochrome c release, caspase activation, and PARP cleavage were assessed.
Main Results:
- Zinc treatment caused cytochrome c translocation from mitochondria to cytosol in PC-3 cells.
- Activation of caspase-9 and caspase-3, and PARP cleavage were observed following zinc exposure.
- Zinc-accumulating rat prostate cells showed increased apoptosis, while non-accumulating human cells did not.
Conclusions:
- High intracellular zinc accumulation in prostate cells induces mitochondrial apoptogenesis.
- This represents a novel physiological role for zinc in regulating prostate cell proliferation.
- Mitochondrial pathways are key mediators of zinc's apoptotic effects in prostate cancer cells.