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Fish-oil-derived eicosapentaenoic acid decreases survivin expression and induces wt-p53 accumulation with caspase-3
M R Sam1, M Esmaeillou1, S Sam1
11 Department of Cellular and Molecular Biotechnology, Institute of Biotechnology, Urmia University, Urmia, Iran.
Background:
Defects in modulating wild-type (wt) p53 and survivin are associated with a resistant disease in acute lymphoblastic leukemia (ALL). Yet, no wt-p53 and survivin modulating drugs have been approved for clinical application in ALL. Here, we investigated if in vitro eicosapentaenoic acid (EPA) concentrations equal to human plasma levels are able to target wt-p53 and survivin.
Methods:
Wt-p53 Molt-4 cells (ALL cell line) were treated with 50, 100, 150, and 200 µM of EPA after which cell number, viability, proliferation rate, survivin expression, wt-p53 accumulation, caspase-3 activation, and apoptosis were evaluated.
Results:
After 48- and 72-h treatments with EPA at concentrations ranging from 50 to 200 µM, cell proliferation rates were measured to be 71.5-32.6% and 68.2-13.7% and metabolic activities were measured to be 77-44% and 71-26%, respectively. Treatment with 50-200 µM of EPA for 48 h resulted in 14.1-74.6% and 69.5-45.5% decreases in survivin mRNA and protein levels, respectively. EPA induced 1.3-6 and 1.9-20-fold increases in caspase-3 activation and wt-p53 accumulation, respectively. Increase in wt-p53/survivin and caspase-3/survivin ratios from 1 in untreated cells to 20.3 and 5.8 was measured for 150 µM of EPA. Low necrotic rates ranging from 0.3% to 2.8% and an increase in the number of total apoptotic cells (early + late) ranging from 9.8% to 81% were also observed with increasing EPA concentrations.
Conclusion:
EPA induces strongly wt-p53 with a remarkable decrease in survivin expression, representing an attractive compound to modulate wt-p53 and survivin in ALL cells.
Insights
Eicosapentaenoic acid (EPA) effectively targets wild-type p53 and survivin in acute lymphoblastic leukemia (ALL) cells. This study shows EPA induces apoptosis and reduces proliferation, offering a potential therapeutic strategy for resistant ALL.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Dysregulation of wild-type p53 (wt-p53) and survivin is linked to treatment resistance in acute lymphoblastic leukemia (ALL).
- Currently, no approved drugs effectively modulate wt-p53 and survivin for ALL treatment.
- Eicosapentaenoic acid (EPA) is investigated for its potential to target these pathways at concentrations found in human plasma.
Purpose of the Study:
- To investigate the in vitro effects of eicosapentaenoic acid (EPA) on wt-p53 and survivin modulation in ALL cells.
- To evaluate EPA's impact on cell viability, proliferation, apoptosis, and related molecular markers.
Main Methods:
- Molt-4 ALL cells (expressing wt-p53) were treated with varying concentrations of EPA (50–200 µM).
- Evaluated parameters included cell number, viability, proliferation, survivin mRNA and protein expression, wt-p53 accumulation, caspase-3 activation, and apoptosis.
- Measurements were taken at 48 and 72 hours post-treatment.
Main Results:
- EPA significantly reduced ALL cell proliferation and metabolic activity in a dose- and time-dependent manner.
- EPA treatment led to substantial decreases in survivin mRNA and protein levels.
- EPA induced significant increases in caspase-3 activation and wt-p53 accumulation, enhancing the wt-p53/survivin and caspase-3/survivin ratios.
- EPA treatment markedly increased apoptosis in ALL cells with minimal necrosis.
Conclusions:
- Eicosapentaenoic acid (EPA) effectively induces wt-p53 accumulation and significantly downregulates survivin expression in ALL cells.
- EPA demonstrates potential as a therapeutic agent for modulating wt-p53 and survivin pathways in acute lymphoblastic leukemia.
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