eicosapentaenoic acid / ROS Cancer Research Results

EPA, eicosapentaenoic acid: Click to Expand ⟱

Features:

Eicosapentaenoic Acid (EPA)
– An omega-3 polyunsaturated fatty acid (PUFA) primarily found in marine sources such as fatty fish and algae.
– EPA is involved in the synthesis of eicosanoids, which are signaling molecules that modulate inflammatory processes.

Eicosapentaenoic acid — Eicosapentaenoic acid is a 20-carbon, five-double-bond long-chain omega-3 polyunsaturated fatty acid formally designated 20:5n-3. Its ethyl-ester pharmaceutical form is icosapent ethyl. EPA is obtained mainly from oily fish, marine oils and microalgae, with limited endogenous formation from alpha-linolenic acid. It is a dietary lipid, membrane constituent and precursor of less-inflammatory eicosanoids and specialized pro-resolving mediators. EPA is an approved cardiometabolic drug component but is not an approved anticancer therapy.

Primary mechanisms (ranked):

Remodels membrane phospholipid composition by partly replacing arachidonic acid, thereby altering lipid-raft organization, receptor signalling and the substrate pool available for eicosanoid synthesis.
Shifts lipid-mediator production toward generally less-inflammatory prostaglandins, thromboxanes and leukotrienes and toward E-series resolvins that promote inflammatory resolution.
Suppresses inflammatory signalling, including NF-κB, COX-2, PGE2 and selected cytokines, with effects dependent on tissue, stimulus, EPA dose and treatment duration.
In susceptible cancer cells, increases incorporation of highly peroxidizable omega-3 lipid into membranes, promoting lipid peroxidation, mitochondrial stress, apoptosis and potentially ferroptotic vulnerability.
Modulates PI3K/Akt, MAPK, cell-cycle and apoptosis pathways in experimental cancer models, although the direction and magnitude vary substantially by cancer type and exposure conditions.
May modify tumour-associated inflammation, cachexia-related proteolysis and lipolysis and treatment tolerance; human results are inconsistent and EPA alone has not demonstrated reliable antitumour efficacy.
substantial evidence that EPA can reduce inflammatory signalling, although the effect is strongest in people or cells with pre-existing inflammatory activation.
May enhance chemotherapy or radiotherapy responses in selected experimental models through membrane remodelling and oxidative sensitization, but this remains adjunctive and context-dependent.

Bioavailability / PK relevance: Oral EPA is absorbed with dietary lipid, transported largely through intestinal lymph and incorporated into plasma phospholipids, triglycerides and cholesteryl esters. Icosapent ethyl is hydrolysed during absorption; peak plasma EPA occurs at approximately 5 hours, more than 99% of circulating unesterified EPA is protein-bound, and the reported terminal plasma half-life is approximately 89 hours. Biological effects depend more on sustained membrane incorporation and achieved omega-3 status than on a brief free-plasma concentration. Oxidation, formulation, meal composition and EPA content strongly affect exposure.

In-vitro vs systemic exposure relevance: Many direct anticancer experiments use approximately 25–200 µM EPA for one or more days. These conditions can produce membrane loading and lipid peroxidation greater than ordinary dietary exposure, while less than 1% of circulating EPA is present as unesterified fatty acid. Acute free-EPA concentrations used in vitro therefore commonly exceed physiologically available unbound exposure; longer-term membrane incorporation is the more clinically relevant comparison.

Clinical evidence status: RCT evidence supports prescription icosapent ethyl for selected cardiovascular and hypertriglyceridaemia indications, not cancer treatment. In oncology, evidence consists of preclinical studies, nutritional-intervention trials and small-to-moderate adjunct studies involving cachexia, body composition, inflammatory biomarkers or treatment tolerance. Several controlled cachexia trials were negative or inconclusive, while some nutritional studies reported preservation of weight or lean mass. EPA should be classified as an investigational nutritional adjunct in cancer rather than a demonstrated anticancer agent.

Safety / deployment status: Dietary EPA and conventional fish-oil doses are generally well tolerated, but concentrated prescription EPA can increase bleeding events and atrial fibrillation or flutter, particularly in predisposed patients or those using antiplatelet or anticoagulant drugs. Gastrointestinal effects, fish-derived allergen concerns, product oxidation and variable supplement purity are additional constraints. The FDA-approved icosapent ethyl dose is 4 g/day for its labelled cardiovascular or triglyceride indications; this dose should not be extrapolated as an anticancer regimen.

Mechanistic Effects of EPA

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Membrane phospholipid and arachidonic-acid competition	EPA incorporation ↑; arachidonic-acid-derived signalling ↓	EPA incorporation ↑; inflammatory lipid substrate availability ↓	G	Membrane remodelling and altered signal transduction	Central mechanism requiring sustained exposure; dependent on baseline fatty-acid composition.
2	Eicosanoids and E-series resolvins	Pro-inflammatory prostanoid and leukotriene signalling ↓; resolution mediators ↑	Inflammatory resolution ↑; excessive leukocyte activation ↓	R/G	Inflammation modulation	EPA competes with arachidonic acid and serves as a precursor for less-inflammatory and pro-resolving mediators.
3	NF-κB COX-2 PGE2 cytokine axis	NF-κB ↓; COX-2 ↓; PGE2 ↓; IL-6 and TNF signalling ↓ (context-dependent)	Stimulus-induced NF-κB and cytokine production ↓	R/G	Suppression of inflammatory and tumour-promoting signalling	Direction is not universal; some immune contexts show mixed or biphasic regulation.
4	Lipid peroxidation and ferroptotic vulnerability	Peroxidizable membrane PUFA ↑; lipid ROS ↑; ferroptotic susceptibility ↑ (model-dependent)	Lipid peroxidation ↔ or ↑ when antioxidant capacity is insufficient	R/G	Oxidative membrane damage in susceptible tumour cells	Potential therapeutic leverage but also a stability and normal-tissue constraint; strongly affected by antioxidants and iron availability.
5	Mitochondrial stress and apoptosis	Mitochondrial membrane dysfunction ↑; caspase activation ↑; apoptosis ↑	Mitochondrial function ↔ or protected at nutritional exposure; oxidative injury possible at high concentration	R/G	Programmed cell death	Most convincing in cell and animal models using sustained, relatively high EPA exposure.
6	PI3K Akt MAPK and cell-cycle signalling	Akt survival signalling ↓; proliferation ↓; cell-cycle arrest ↑ (model-dependent)	Stress and metabolic signalling modulation ↔	R/G	Reduced proliferation and survival signalling	Secondary mechanism with substantial tumour-type and concentration dependence.
7	Cachexia-associated inflammation and catabolism	Tumour-derived inflammatory and catabolic signalling ↓ (indirect)	Muscle proteolysis ↓; lipolysis ↓; lean-mass preservation ↑ (inconsistent)	G	Potential nutritional and metabolic support	Preclinical rationale is stronger than clinical efficacy; several randomized trials did not show clear benefit.
8	Chemosensitization	Drug-induced apoptosis or oxidative injury ↑ (context-dependent)	Treatment toxicity ↔ or ↓ in selected nutritional studies	G	Potential adjunctive treatment modulation	Not established as a standard chemosensitizer; effects may differ by drug, tumour genotype and antioxidant environment.
9	Clinical Translation Constraint	Direct tumour exposure uncertain; clinical antitumour activity unproven	Bleeding risk ↑; atrial fibrillation risk ↑; gastrointestinal intolerance possible	G	Limits translation from experimental models	Formulation, oxidation, meal conditions, baseline omega-3 status, tumour heterogeneity and use of EPA-DHA mixtures complicate interpretation.

P: 0–30 min R: 30 min–3 hr G: >3 hr

Lipid peroxidation and ROS: EPA incorporation increases the abundance of highly peroxidizable membrane polyunsaturated lipids. In susceptible cancer-cell models, EPA increases intracellular ROS and lipid-peroxidation products, contributing to mitochondrial dysfunction, apoptosis or necrosis. The effect is dose-dependent and strongly modified by iron availability, glutathione, glutathione peroxidase activity, vitamin E and other antioxidant defenses. Direct evidence is primarily preclinical and is not consistent across all cancer types.

Membrane EPA incorporation ↑; ROS ↑; lipid peroxidation ↑; apoptosis or necrosis ↑ (dose-dependent) (model-dependent)

Normal cells, Stress-induced ROS ↓; NADPH oxidase activity ↓; basal ROS ↔; lipid peroxidation ↔ or ↑ under strongly pro-oxidant conditions

ROS, Reactive Oxygen Species: Click to Expand ⟱

Source: HalifaxProj (inhibit)

Type:

Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination


Item  ROS↑  NRF2  Condition  Mechanism Class  Remarks  

ROS">Piperlongumine
+++  ↓  [D][T]  ROS-dominant
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



ROS">Copper (ionic / nano)
+++ ↓ [Fe][F] ROS-dominant
Fenton-type redox chemistry



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



ROS">Alpha-lipoic acid (ALA)
± ↑ [D][M] NRF2-dominant
Antioxidant at low dose



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



ROS">Quercetin
± ↑/↓ [D][Fe] NRF2-dominant
GSH-dependent cycling



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

6793-

EPA,

Contribution of Pyk2 pathway and reactive oxygen species (ROS) to the anti-cancer effects of eicosapentaenoic acid (EPA) in PC3 prostate cancer cells

in-vitro,

Pca,

PC3

tumCV↓, ERK↓, PTK2B / PYK2↓, TumCG↓, ROS↑, TumCMig↓, TumCI↓,

6794-

EPA,

EPA, an omega-3 fatty acid, induces apoptosis in human pancreatic cancer cells: role of ROS accumulation, caspase-8 activation, and autophagy induction

in-vitro,

BC,

vitro+vivo,

PC,

MIA PaCa-2

ROS↑, Casp8↑, Apoptosis↑, ROS↑, TumCG↓, TumCD↑, eff↑,

6795-

EPA,

Necrosis and apoptosis in lymphoma cell lines exposed to eicosapentaenoic acid and antioxidants

in-vitro,

lymphoma,

ROS↑, Necroptosis↑,

6796-

EPA,

Effect of eicosapentaenoic acid and other fatty acids on the growth in vitro of human pancreatic cancer cell lines

in-vitro,

PC,

MIA PaCa-2

in-vitro,

Pca,

PANC1

TumCG↓, eff↓, lipid-P↑, tumCV↓, ROS↑,

6797-

EPA,

Effects of cellular redox balance on induction of apoptosis by eicosapentaenoic acid in HT29 colorectal adenocarcinoma cells and rat colon in vivo

in-vivo,

Colon,

HT29

we investigated involvement of caspase enzymes and cellular redox balance in the induction of apoptosis by eicosapentaenoic acid (EPA) in HT29 cells, and in rat colon in vivo

tumCV↓, Casp3↑, eff↓, eff↑, Apoptosis↑, ROS↑,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 2, eff↑, 2,
Total Targets: 15

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

5 eicosapentaenoic acid

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:259  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

eicosapentaenoic acid / ROS Cancer Research Results

Mechanistic Effects of EPA

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Pathway results for Effect on Normal Cells:

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