Eugenol / ROS Cancer Research Results

Eug, Eugenol: Click to Expand ⟱
Features:

Eugenol — Eugenol is a naturally occurring phenylpropanoid and volatile aromatic phenol most strongly associated with clove oil from Syzygium aromaticum. Eugenol is a phenolic aromatic ingredient that is chiefly derived from clove oil. It is formally classified as a small-molecule phytochemical, essential-oil constituent, food-flavouring agent, and experimental anticancer adjunct rather than an approved oncology drug. Standard abbreviations include EUG and 4-allyl-2-methoxyphenol. It is also present in cinnamon, basil, bay, nutmeg, and other aromatic plants. The oncology evidence is mainly preclinical, with strongest support for apoptosis induction, PI3K/Akt suppression, anti-metastatic effects, and chemo/radiosensitization in cell and animal models. clove oil has been advertised as a dental pain-relieving agent and germicide, and is used in mouthwashes and pharmaceutical drugs. Eugenol (4-allyl (-2-mthoxyphenol)), a phenolic natural compound available in honey and in the essential oils of different spices such as Syzgium aromaticum (clove), Pimenta racemosa (bay leaves), and Cinnamomum verum (cinnamon leaf).
-eugenol is the major ingredient of three spices (i.e. clove, cinnamon,and nutmeg)
-clear to pale yellow liquid with an oily consistency and a spicy aroma. It is sparingly soluble in water and well soluble in organic solvents.
-entering the systemic circulation within 30-60 minutes, paradoxically limits it therapeutic effectiveness.

Primary mechanisms (ranked):

  1. Induction of intrinsic and extrinsic apoptosis through mitochondrial dysfunction, Bax/Bcl-2 shift, cytochrome-c release, caspase activation, and PARP cleavage.
  2. Suppression of PI3K/Akt/mTOR and related survival signalling, including FOXO3a-linked autophagy/apoptosis in breast cancer models.
  3. Anti-inflammatory transcriptional modulation, especially ↓ NF-κB, ↓ COX-2, ↓ inflammatory cytokine signalling, and context-dependent STAT3/IL-6 axis suppression.
  4. Anti-metastatic and anti-invasive activity through ↓ MMP-2/MMP-9, ↓ migration, ↓ invasion, and reduced epithelial-mesenchymal transition markers in selected models.
  5. Anti-angiogenic effects through ↓ VEGF-linked signalling and reduced invasion/angiogenesis markers in gastric and other cancer models.
  6. ROS redox modulation with model-dependent pro-oxidant stress in cancer cells and antioxidant/anti-inflammatory effects in non-malignant contexts.
  7. Chemosensitization and radiosensitization, reported preclinically with cisplatin, gemcitabine, and ionizing radiation, but not clinically established.

Bioavailability / PK relevance: Eugenol is rapidly absorbed and extensively metabolized, mainly through conjugation pathways, so systemic exposure is transient and formulation-dependent. Its volatility, lipophilicity, rapid metabolism, and local irritation risk make delivery strategy important. Nanoemulsions, encapsulation, and conjugated delivery systems are being explored preclinically to improve stability, exposure, and tumour delivery.

In-vitro vs systemic exposure relevance: Many in-vitro anticancer studies use micromolar-to-high-micromolar concentrations that may exceed freely achievable systemic exposure after ordinary dietary or flavouring-level intake. Low-dose mechanistic reports exist in some breast cancer models, but translation remains uncertain. Essential-oil or clove-derived exposure should not be equated with purified eugenol pharmacology because source composition, dose, and route strongly affect exposure.

Clinical evidence status: Preclinical. Eugenol has cell-line and animal-model anticancer evidence, plus limited adjunctive clinical-context use in aromatherapy or topical/dental products, but there is no established clinical evidence supporting eugenol as a cancer treatment. Registry-visible oncology studies involving essential oils generally assess symptom support or mixtures, not purified eugenol as an anticancer therapeutic.

Eugenol Cancer Mechanism Table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial apoptosis and caspases ↑ Bax, ↑ cytochrome-c, ↑ caspase-3/8/9, ↓ Bcl-2, ↓ PARP integrity Mixed; cytoprotection at low exposure but irritation/cytotoxicity at high exposure R/G Apoptotic tumour-cell killing Core and most reproducible anticancer axis across breast, cervical, gastric, lung, and other models.
2 PI3K Akt mTOR survival signalling ↓ PI3K/Akt, ↓ mTOR signalling, ↑ FOXO3a activity, ↑ autophagy/apoptosis Context-dependent R/G Reduced survival signalling and increased treatment vulnerability Highly relevant in breast cancer and lung cancer models; may overlap with HER2/PI3K-Akt effects.
3 NF-κB COX-2 inflammatory signalling ↓ NF-κB, ↓ COX-2, ↓ inflammatory cytokine signalling ↓ inflammatory signalling in non-malignant inflammatory contexts R/G Anti-inflammatory and anti-survival transcriptional pressure Important bridge between anticancer and general anti-inflammatory pharmacology.
4 MMP invasion and metastasis ↓ MMP-2, ↓ MMP-9, ↓ migration, ↓ invasion Context-dependent G Anti-invasive and anti-metastatic activity Mechanistically meaningful for breast, fibrosarcoma, gastric, and lung cancer models.
5 Angiogenesis and VEGF-linked signalling ↓ VEGF-linked angiogenic markers, ↓ invasion-associated vascular support Context-dependent; excessive exposure may irritate tissues G Reduced tumour vascularization support Best supported in animal carcinogenesis and metastasis-associated models rather than clinical oncology.
6 Cell cycle arrest ↑ p21, ↑ p27, ↓ cyclin-linked proliferation, S-phase or G2/M effects depending on model Context-dependent G Reduced proliferation Secondary but common contributor to antiproliferative activity.
7 Mitochondrial ROS redox stress ↑ ROS or redox stress in some cancer models; antioxidant effects in others Often ↓ oxidative stress at low exposure; irritation or toxicity possible at high exposure P/R/G Context-dependent redox modulation Do not tag simply as antioxidant. Cancer-cell effect can be pro-oxidant, antioxidant, or mixed depending on dose, timing, and model.
8 NRF2 antioxidant response Mixed or context-dependent; not a primary anticancer-defining axis Potential ↑ cytoprotective antioxidant response in non-malignant stress models G Secondary redox adaptation Include only as secondary/contextual unless a specific study demonstrates NRF2-dependent cancer-cell modulation.
9 Glycolysis and metabolic reprogramming Metabolomic shifts reported; likely ↓ proliferative metabolic fitness in selected CRC/oral cancer contexts Unclear G Metabolic stress Mechanistically interesting but less mature than apoptosis, PI3K/Akt, and invasion axes.
10 Chemosensitization ↑ cisplatin cytotoxicity, ↑ gemcitabine activity, ↑ apoptosis Potential normal-cell toxicity not adequately defined R/G Adjunctive treatment sensitization Preclinical only; promising but insufficient for clinical-use claims.
11 Radiosensitization ↑ ionizing-radiation cytotoxicity in cervical and oral cancer models Normal-tissue protection versus sensitization remains unresolved R/G Radiation response enhancement Preclinical only; should be tagged as experimental radiosensitizer, not clinically validated.
12 Clinical Translation Constraint In-vitro exposure may exceed realistic free systemic levels High-dose clove oil/eugenol can irritate mucosa and has overdose hepatotoxicity risk G Limits direct translation Major constraints are rapid metabolism, dose-limited tolerability, formulation dependence, lack of oncology trials, and distinction between food-level GRAS use and therapeutic dosing.

TSF legend: P: 0–30 min; R: 30 min–3 hr; G: >3 hr
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






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






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






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






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






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






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






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


Scientific Papers found: Click to Expand⟱
6377- Eug,    Pharmacological Properties and Health Benefits of Eugenol: A Comprehensive Review
- Review, Var, NA - Review, AD, NA
*Inflam↓, *Bacteria↓, ChemoSen↑, *selectivity↑, ROS⇅, TumCG↓, MMP↓, antiOx⇅, *antiOx↑, *BBB↑, *neuroP↑, *BDNF↑, *Aβ↓, *Ca+2↓, *5LO↓, *MAOA↓, other↑,
6378- Eug,    Effects of Eugenol on the Central Nervous System: Its Possible Application to Treatment of Alzheimer's Disease, Depression, and Parkinson's Disease
- Review, AD, NA
*other↑, *Aβ↓, *BDNF↑, *MAOA↑, *toxicity↓, *Ca+2↓, *antiOx↑, *ROS↓, *lipid-P↓, *neuroP↑, *PGE2↓, *COX2↓, *5LO↓,
6381- Eug,    Biological Properties and Prospects for the Application of Eugenol—A Review
- Review, Var, NA
*eff↑, *BioAv↝, *BioAv↝, *BioAv↑, *antiOx↑, *AntiAg↑, *Inflam↓, *AntiBio↑, *MAOA↓, *neuroP↑, *ROS↓, *RNS↓, *eff↑, NF-kB↓, PGE2↓, COX2↓, TumCCA↑, Apoptosis↑, TumCMig↓, TumCI↓, tumCV↓, PI3K↓, Akt↓, MMPs↓, ChemoSen↑, ALDH↓, *Pain↓, *VGSC↓, *IL1β↓, *IL6↓, *TNF-α↓, *iNOS↓, *5LO↓, *chemoPv↑,
6388- Eug,    Eugenol’s anti-cancer properties, its modulation of signalling pathways, and cascades across various cancers: A review
- Review, Var, NA
Dose↝, AntiCan↑, *Inflam↓, *cardioP↑, *neuroP↑, angioG↓, TumMeta↓, *BioAv↑, *eff↑, *toxicity↝, antiNeop↑, TumCCA↑, Apoptosis↑, *antiOx↑, *lipid-P↓, *ROS↓, *SOD↑, *Catalase↑, *GSTs↑, *GPx↑, *iNOS↓, *COX2↓, *IL6↓, *TNF-α↓, *AntiArt↑, *Bacteria↓, TumAuto↑, PI3K↓, Akt↓, FOXO3↝, BAX↑, mTOR↓, NF-kB↓, P53↑, TumCG↓, CSCs↓, CD44↓, EpCAM↓, NOTCH1↓, OCT4↓, Bcl-2↓, PDK1↓, HER2/EBBR2↓, BAD↓, cycD1/CCND1↓, ROS↑, Casp3↑, selectivity↑, MMP2↓, MMP9↓, TIMP1↑, VEGF↓, VEGFR1↓, RECK↑, TIMP2↑, DNAdam↑, MMP↓, Thiols↓, PARP↑, *Pain↓, E2Fs↓, survivin↓,
6389- Eug,    Molecular Insights into the Management of Eugenol's Anticancer Action Against Colon Cancer: A Detailed Review
- Review, Colon, NA
Apoptosis↓, TumCCA↓, Inflam↓, TumMeta↓, BioAv↑, eff↓, Half-Life↓, *ROS↓, *RNS↓, *SOD↓, *Catalase↑, *GSTs↑, *MAOA↓, *neuroP↑, *DNAdam↓, Apoptosis↑, ROS↑, selectivity↑, MMP↓, Cyt‑c↓, Casp3↑, Casp9↑, TumCD↑, BAX↑, BAD↑, APAF1↑, Bcl-2↓, Bcl-xL↓, P53↑, cl‑PARP↑, TumCCA↑, cycD1/CCND1↓, CycB/CCNB1↓, CDK2↓, CDK4↓, P21↑, p27↑, NF-kB↓, COX2↓, PGE2↓, MAPK↓, PI3K↓, Akt↓, mTOR↓, MMPs↓, EMT↓, Snail↓, Slug↓, Zeb1↓, E-cadherin↑, ChemoSen↑,
6390- Eug,    Molecular mechanisms of eugenol as an antitumour bioactive compound: A comprehensive review
- Review, Var, NA
TumCCA↑, angioG↓, TumMeta↓, tumCV↓, Casp3↑, Casp6↑, DFF45↑, PARP↑, ROS↑, Cyt‑c↑, MPT↑, *ROS↓, NF-kB↓, COX2↓, 5LO↓, EMT↓, Snail↓, E-cadherin↑, Vim↓, PI3K↓, Akt↓, mTORC2↓, TumAuto↑, FOXO3↓, Apoptosis↑, ChemoSen↑, RadioS↑, DNMT1↓, DNMT3A↓,
6356- Eug,  Cin,    Investigating the Molecular Mechanisms of the Anticancer Effects of Eugenol and Cinnamaldehyde Against Colorectal Cancer (CRC) Cells In Vitro
- in-vitro, CRC, SW-620 - in-vitro, CRC, Caco-2 - in-vitro, Nor, NCM460
P21↑, ChemoSen↑, Casp3↑, IL4↓, IL8↓, ROS↑, NRF2↑, HO-1↑, EMT↓,
6323- Eug,    Eugenol: An Insight Into the Anticancer Perspective and Pharmacological Aspects
- Review, Var, NA - Review, Arthritis, NA
*AntiCan↑, *AntiDiabetic↑, *cardioP↑, *toxicity↝, *GutMicro↑, *neuroP↑, *BioAv⇅, *BioAv↝, *antiOx↑, *Inflam↑, *AntiArt↑, *TNF-α↓, *IL6↓, *IL10↓, *GSH↑, *GPx↑, *Catalase↑, *MDA↓, *TAC↑, TumCMig↓, TumCI↓, Akt↑, FOXO3↑, Casp3↑, Casp9↑, P21↑, angioG↓, TumCI↓, Apoptosis↑, NF-kB↓, eff↑, eff↑, ChemoSen↑, NA↑, Casp3↑, Casp9↑, *AntiDiabetic↑, *glucose↓, *ROS↓, *Inflam↓, *MDA↓, *GSH↑, *BioAv↑,
6325- Eug,    Anticancer Properties of Eugenol: A Review
- Review, Var, NA
*antiOx↑, *AntiCan↑, *Inflam↓, TumCD↑, TumCCA↑, TumCMig↓, TumMeta↓, angioG↓, ChemoSen↑, chemoP↑, *BioAv↝, *BioAv↑, *BioAv↑, *BioAv↑, *Bacteria↓, *ROS↓, *IL6↓, *COX2↓, *TNF-α↓, *lipid-P↓, *SOD1↑, *Catalase↑, *GPx1↑, *GSTs↑, ROS↑, MMP↓, Apoptosis↑, COX2↓, TumCCA↑, E2Fs↓, PI3K↓, Akt↓, MMPs↓, CSCs↓, OCT4↓, CD44↓, EpCAM↓, NOTCH1↓, TumVol↓, Casp3↑, P53↑, cl‑PARP↑, MMP2↓, MMP9↓, TIMP1↑, ALDH↓, NF-kB↓, *toxicity↓,
6330- Eug,    Molecular Mechanisms of Action of Eugenol in Cancer: Recent Trends and Advancement
- Review, Var, NA
TumCD↑, TumCCA↑, AntiCan↑, Apoptosis↑, angioG↓, TumCI↓, TumMeta↓, ChemoSen↑, ALDH↓, NF-kB↓, IL6↓, IL8↓, BAX↑, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, Bcl-2↓, MMP2↓, MMP9↓, EMT↓, N-cadherin↓, Snail↓, E-cadherin↑, SOX2↓, ROS↑, PCNA↓, MMP1↓, Cyt‑c↑, LDH↑, CSCs↓, OCT4↓, NOTCH1↓, EpCAM↓, CD44↓, HER2/EBBR2↓, VEGF↓, TIMP2↑, eff↑, Ca+2↑, TumVol↓, DNAdam↑, GSH↓, H2O2↑, lipid-P↑,
6333- Eug,  Cisplatin,  Rad,    Eugenol Exerts Apoptotic Effect and Modulates the Sensitivity of HeLa Cells to Cisplatin and Radiation
- in-vitro, Cerv, HeLa
TumCP↓, LDH↝, ChemoSen↑, RadioS↑, Casp3↑, BAX↑, Cyt‑c↑, Casp9↑, Bcl-2↓, COX2↓, IL1β↓, ROS↑, NF-kB↓, COX2↓, TumCCA↓, Thiols↓, GSH↓,
6335- Eug,    Eugenol with antioxidant activity inhibits MMP-9 related to metastasis in human fibrosarcoma cells
- in-vitro, Nor, NA
*H2O2↓, *ROS↓, *lipid-P↓, MMP9↓, TIMP1↓, *ROS↓, *antiOx↑,
6338- Eug,    Tumor suppressive roles of eugenol in human lung cancer cells
- in-vitro, Lung, A549
tumCV↓, TumCMig↓, TumCI↓, Akt↓, MMP2↓, *lipid-P↓, *COX2↓, *ROS↓, PI3K↓,
6341- Eug,    A Metabolomic Investigation of Eugenol on Colorectal Cancer Cell Line HT-29 by Modifying the Expression of APC, p53, and KRAS Genes
- NA, Colon, HT29
*antiOx↑, ROS↑, tumCV↓, P53↑, APC↑, KRAS↓, FAO↓, Glycolysis↓,
6355- Eug,    Pharmacological and Toxicological Properties of Eugenol
- Review, Var, NA
*Inflam↓, *antiOx↑, *NF-kB↓, *AntiArt↑, *lipid-P↓, *GSH↑, ROS↑, GSH↓, ChemoSen↑, Apoptosis↑, MMP↓, TumCG↓, TumCCA↑,

Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned ⓘ

NA↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx⇅, 1,   GSH↓, 3,   H2O2↑, 1,   HO-1↑, 1,   lipid-P↑, 1,   NRF2↑, 1,   ROS↑, 9,   ROS⇅, 1,   Thiols↓, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 5,   MPT↑, 1,  

Core Metabolism/Glycolysis ⓘ

FAO↓, 1,   Glycolysis↓, 1,   LDH↑, 1,   LDH↝, 1,   PDK1↓, 1,  

Cell Death ⓘ

Akt↓, 6,   Akt↑, 1,   APAF1↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 8,   BAD↓, 1,   BAD↑, 1,   BAX↑, 4,   Bcl-2↓, 4,   Bcl-xL↓, 1,   Casp3↑, 8,   cl‑Casp3↑, 1,   Casp6↑, 1,   Casp9↑, 4,   cl‑Casp9↑, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 3,   MAPK↓, 1,   p27↑, 1,   survivin↓, 1,   TumCD↑, 3,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,  

Transcription & Epigenetics ⓘ

other↑, 1,   tumCV↓, 4,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DFF45↑, 1,   DNAdam↑, 2,   DNMT1↓, 1,   DNMT3A↓, 1,   P53↑, 4,   PARP↑, 2,   cl‑PARP↑, 3,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   E2Fs↓, 2,   P21↑, 3,   TumCCA↓, 2,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 3,   CD44↓, 3,   CSCs↓, 3,   EMT↓, 4,   EpCAM↓, 3,   FOXO3↓, 1,   FOXO3↑, 1,   FOXO3↝, 1,   mTOR↓, 2,   mTORC2↓, 1,   NOTCH1↓, 3,   OCT4↓, 3,   PI3K↓, 6,   SOX2↓, 1,   TumCG↓, 3,  

Migration ⓘ

5LO↓, 1,   APC↑, 1,   Ca+2↑, 1,   E-cadherin↑, 3,   KRAS↓, 1,   MMP1↓, 1,   MMP2↓, 4,   MMP9↓, 4,   MMPs↓, 3,   N-cadherin↓, 1,   RECK↑, 1,   Slug↓, 1,   Snail↓, 3,   TIMP1↓, 1,   TIMP1↑, 2,   TIMP2↑, 2,   TumCI↓, 5,   TumCMig↓, 4,   TumCP↓, 1,   TumMeta↓, 5,   VEGFR1↓, 1,   Vim↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 6,   IL1β↓, 1,   IL4↓, 1,   IL6↓, 1,   IL8↓, 2,   Inflam↓, 1,   NF-kB↓, 8,   PGE2↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 10,   Dose↝, 1,   eff↓, 1,   eff↑, 3,   Half-Life↓, 1,   RadioS↑, 2,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 2,   IL6↓, 1,   KRAS↓, 1,   LDH↑, 1,   LDH↝, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   antiNeop↑, 1,   chemoP↑, 1,   TumVol↓, 2,  
Total Targets: 123

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

AntiArt↑, 3,   AntiBio↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 9,   Catalase↑, 4,   GPx↑, 2,   GPx1↑, 1,   GSH↑, 3,   GSTs↑, 3,   H2O2↓, 1,   lipid-P↓, 6,   MDA↓, 2,   RNS↓, 2,   ROS↓, 10,   SOD↓, 1,   SOD↑, 1,   SOD1↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↓, 1,  

Cell Death ⓘ

iNOS↓, 2,  

Transcription & Epigenetics ⓘ

other↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

VGSC↓, 1,  

Migration ⓘ

5LO↓, 3,   AntiAg↑, 1,   Ca+2↓, 2,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   IL10↓, 1,   IL1β↓, 1,   IL6↓, 4,   Inflam↓, 6,   Inflam↑, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 4,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 2,   MAOA↓, 3,   MAOA↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 6,   BioAv⇅, 1,   BioAv↝, 4,   eff↑, 3,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,   IL6↓, 4,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiDiabetic↑, 2,   cardioP↑, 2,   chemoPv↑, 1,   neuroP↑, 6,   Pain↓, 2,   toxicity↓, 2,   toxicity↝, 2,  

Infection & Microbiome ⓘ

Bacteria↓, 3,  
Total Targets: 55

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
15 Eugenol
1 Cinnamon
1 Cisplatin
1 Radiotherapy/Radiation
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#:399  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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