Table 6.
n-3 PUFA and breast cancer risk: cell culture studies.
| Cell Type | n-3 PUFA Source | Main Finding | Mechanism | Reference |
|---|---|---|---|---|
| MDA-MB-231 | EPA/DHA alone: 75 μM or 100 μM EPA + DHA combination: 45 μM EPA + 30 μM DHA or 60 μM EPA + 40 μM DHA (in presence/absence of LA) | ↓ cell viability, cell proliferation ↑ DNA fragmentation, cell apoptosis DHA was more potent than EPA | ↓ pAkt ↓ NF-κB and DNA binding activity | [96] |
| MDA-MB-231 | 0.5–2.5 μg/mL of EPA, DHA (1.7–8.2 μM EPA, 1.5–7.6 μMDHA) | ↓ tumor cells growth (DHA > EPA, dose-dependent) | ↓ LA composition in cell lipids ↓ AA-derived eicosanoid synthesis | [121] |
| MDA-MB-231 | EPA/DHA alone: 75 μM or 100 μM EPA + DHA combination: 45 μM EPA + 30 μM DHA or 60 μM EPA + 40 μM DHA (in presence/absence of LA) | ↓cell growth (48%–62%) | ↑ EPA, DHA, DPA and total n-3 in lipid rafts ↓ EGFR levels ↑ pEGFR | [22] |
| MDA-MB-231 MCF-7 | EPA (230 μM), DHA (200 μM) | ↓ cell viability ↑ cell apoptosis | ↓ Bcl-2 ↑pro-caspase-8 ↓ pEGFR ↓ EGFR (only DHA) ↓ AA ↑ EPA, DPA, DHA in total cell lipids | [71] |
| MDA-MB-231 MCF-7 | 3–100 μM of EPA, DHA | At 50 μM EPA, 30 μM DHA ↑ cell apoptosis ↓ cell growth At 50 μM EPA, DHA ↑ G2/M duration DHA was more potent than EPA | ↓ phosphorylation of cyclin B1 ↓ activity of CDK1-cyclin B1 | [86] |
| MCF-7 | 100 μM of EPA, DHA | ↓ cell growth (30% by EPA, 54% by DHA) ↑ cell differentiation (30% by EPA, 65% by DHA) No significant effects on cell apoptosis and cell cycle DHA was more potent than EPA | ↑ PPARγ (DHA only) | [125] |
| MCF-7 MCF-10A | 6–30 μM of ALA, EPA, DHA | All n-3 PUFA ↓ MCF-7 cell growth (EPA, DHA > ALA, dose-dependent) AA ↓ MCF-7 cell growth (similar as ALA) | NA | [122] |
| ER+ and ER− cells | 20 μg/mL of ALA, EPA, DHA (72 μM ALA, 66 μM EPA, 61 μM DHA) | EPA, DHA ↓ cell proliferation (all cell lines) ALA ↓ estrogen independent BC cell proliferation | ↑ lipid peroxidation | [124] |
↑: increase; ↓: decrease; NA: not available