G2/M cell-cycle arrest and apoptosis by n-3 fatty acids in a pancreatic cancer model
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Thomas Dekoj1, Sang Lee, Sagun Desai
1Department of Surgery, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
Background:
n-3 fatty acids (n-3FA) have anti-inflammatory and anti-proliferative effects including modulation of pro-inflammatory cascade mediators and cytokine elaboration (i.e., TNF-alpha, IL-10 and PGE(2)) in many cell lines. However, mechanisms of anti-proliferative effects have not been clearly defined.
Materials And Methods:
MIA PaCa-2 pancreatic cancer cells were treated either with n-3FA (treatment), media (control), or n-6FA (control) for all experiments. Cellular proliferation was evaluated with WST-1 reagent. Cells were stained with propidium iodide and analyzed by flow cytometry for cell-cycle arrest, which was further analyzed by cdc2 expression. Membrane and media lipid concentrations were analyzed by high-performance liquid chromatography. Apoptosis was evaluated by AnnexinV-FITC flow cytometry and reconfirmed by poly (ADP-ribose) polymerase (PARP) cleavage and B(cl)-2 expression.
Results:
Propidium iodide flow cytometry of MIA PaCa-2 dosed with n-3FA showed a decrease in cells in G1 phase (11-17%) and an increase cells in G2 phase (7-13%) from controls. cdc2 expression was also decreased at 24 h compared to controls. Annexin-V staining of n-3FA-treated cells demonstrated time-dependent increased apoptosis and PARP cleavage was present only in the n-3FA treatment group. Phospho-B(cl)-2 was also decreased in the n-3FA-treated cells compared to controls.
Conclusions:
Co-incubation of MIA PaCa-2 cells with n-3FA results in both dose- and time-dependent cell-cycle arrest. Cells also progress to cell death via apoptosis. These data support the potential applicability for n-3FA as an antiproliferative and pro-apoptotic strategy.
Insights
Omega-3 fatty acids (n-3FA) were found to inhibit pancreatic cancer cell proliferation by inducing cell-cycle arrest and apoptosis. These findings suggest n-3FA as a potential therapeutic strategy against pancreatic cancer.
Area of Science:
- Oncology
- Molecular Biology
- Nutritional Science
Background:
- Omega-3 fatty acids (n-3FA) exhibit anti-inflammatory and anti-proliferative properties.
- Mechanisms underlying the anti-proliferative effects of n-3FA are not fully understood.
Purpose of the Study:
- To investigate the effects of n-3FA on pancreatic cancer cell proliferation and apoptosis.
- To elucidate the molecular mechanisms of n-3FA-induced anti-proliferative effects.
Main Methods:
- MIA PaCa-2 pancreatic cancer cells were treated with n-3FA.
- Cellular proliferation was assessed using WST-1 assays.
- Cell-cycle arrest was analyzed by flow cytometry and cdc2 expression.
- Apoptosis was evaluated via Annexin-V staining, PARP cleavage, and BCL-2 expression.
Main Results:
- n-3FA treatment led to cell-cycle arrest, with decreased G1 phase and increased G2 phase populations.
- A reduction in cdc2 expression was observed post-treatment.
- n-3FA induced time-dependent apoptosis, evidenced by increased Annexin-V staining and PARP cleavage.
- Decreased phospho-BCL-2 levels indicated an apoptotic pathway activation.
Conclusions:
- n-3FA treatment induces dose- and time-dependent cell-cycle arrest in pancreatic cancer cells.
- n-3FA promotes cancer cell death through apoptosis.
- These findings support the potential of n-3FA as an antiproliferative and pro-apoptotic therapeutic strategy for pancreatic cancer.
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