Differential control of apoptosis by DJ-1 in prostate benign and cancer cells
1Prostate Cancer Research Center, Department of Urology, Health Sciences Center, State University of New York at Stony Brook, Stony Brook, New York 11794-8093, USA. Yaacov.Hod@stonybrook.edu
Abstract:
DJ-1 is a conserved protein reported to be involved in diverse cellular processes ranging from cellular transformation, control of protein-RNA interaction, oxidative stress response to control of male infertility, among several others. Mutations in the human gene have been shown to be associated with an autosomal recessive, early onset Parkinson's disease (PARK7). The present study examines the control of DJ-1 expression in prostatic benign hyperplasia (BPH-1) and cancer (PC-3) cell lines in which DJ-1 abundance differs significantly. We show that while BPH-1 cells exhibit low basal level of DJ-1 expression, stress-inducing agents such as H(2)O(2) and mitomycin C markedly increase the intracellular level of the polypeptide. In contrast, DJ-1 expression is relatively high in PC-3 cells, and incubation with the same cytotoxic drugs does not modulate further the level of the polypeptide. In correlation with the expression of DJ-1, both cytotoxic agents activate the apoptotic pathway in the prostatic benign cells but not in PC-3 cells, which are resistant to their action. We further demonstrate that incubation of BPH-1 cells with TNF-related-apoptosis-inducing-ligand/Apo-2L (TRAIL) also enhances DJ-1 expression and that TRAIL and H(2)O(2) act additively to stimulate DJ-1 accumulation but synergistically in the activation of the apoptotic pathway. Time-course analysis of DJ-1 stimulation shows that while DJ-1 level increases without significant lag in TRAIL-treated cells, there is a delay in H(2)O(2)-treated cells, and that the increase in DJ-1 abundance precedes the activation of apoptosis. Unexpectedly, over-expression of DJ-1 de-sensitizes BPH-1 cells to the action of apoptotic-inducing agents. However, RNA-interference-mediated silencing of DJ-1 expression results in sensitization of PC-3 cells to TRAIL action. These results are consistent with a model in which DJ-1 is involved in the control of cell death in prostate cell lines. DJ-1 appears to play a differential role between cells expressing a low but inducible level of DJ-1 (e.g., BPH-1 cells) and those expressing a high but constitutive level of the polypeptide (e.g., PC-3 cells).
Insights
DJ-1 protein levels influence cell death in prostate cells. Stress increases DJ-1 in benign cells, sensitizing them to apoptosis, while high DJ-1 in cancer cells confers resistance.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- DJ-1 is a protein implicated in various cellular functions, including oxidative stress response and Parkinson's disease (PARK7).
- Prostate cancer cells (PC-3) exhibit different DJ-1 expression levels compared to benign prostatic hyperplasia cells (BPH-1).
Purpose of the Study:
- To investigate the role of DJ-1 expression in the regulation of apoptosis in prostate benign hyperplasia (BPH-1) and prostate cancer (PC-3) cell lines.
- To determine how DJ-1 expression is modulated by cytotoxic agents and its impact on cell death pathways.
Main Methods:
- Comparing DJ-1 expression levels in BPH-1 and PC-3 cells under basal and stress conditions (H2O2, mitomycin C, TRAIL).
- Assessing the activation of the apoptotic pathway in response to cytotoxic agents.
- Manipulating DJ-1 levels via overexpression and RNA interference to observe effects on apoptosis sensitivity.
Main Results:
- BPH-1 cells show low, inducible DJ-1 expression and undergo apoptosis upon stress, while PC-3 cells have high, constitutive DJ-1 and resist apoptosis.
- DJ-1 accumulation precedes apoptosis activation in BPH-1 cells.
- Overexpression of DJ-1 desensitizes BPH-1 cells to apoptosis, whereas DJ-1 silencing sensitizes PC-3 cells to TRAIL-induced apoptosis.
Conclusions:
- DJ-1 plays a differential role in regulating apoptosis in prostate cells based on its expression level.
- Inducible DJ-1 in benign cells contributes to stress-induced apoptosis, while constitutive high DJ-1 in cancer cells promotes resistance.
- DJ-1 is a key regulator of cell death pathways in prostate cancer and benign prostatic hyperplasia.
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