Thymoquinone / ROS Cancer Research Results

TQ, Thymoquinone: Click to Expand ⟱
Features: Anti-oxidant, anti-tumor
Thymoquinone is a bioactive compound found in the seeds of Nigella sativa, commonly known as black seed or black cumin.
Pathways:
-Cell cycle arrest, apoptosis induction, ROS generation in cancer cells
-inhibit the activation of NF-κB, Suppress the PI3K/Akt signaling cascade
-Inhibit angiogenic factors such as VEGF, MMPs
-Inhibit HDACs, UHRF1, and DNMTs

-Note half-life 3-6hrs.
BioAv low oral bioavailability due to its lipophilic nature. Note refridgeration of Black seed oil improves the stability of TQ.
DIY: ~1 part lecithin : 2–3 parts black seed oil : 4–5 parts warm water. (chat ai)
Pathways:
- usually induce ROS production in Cancer cells, and lowers ROS in normal cells
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- May Low AntiOxidant defense in Cancer Cells: NRF2↓(usually contrary), GSH↓ HO1↓(contrary), GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓">ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, VEGF↓, FAK↓, NF-κB↓, CXCR4↓, TGF-β↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMTs↓, EZH2↓, P53↑, HSP↓, Sp proteins↓, TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PDKs↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, α↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Target Axis Direction Label Primary Effect Notes / Cancer Relevance Ref
1 Reactive oxygen species (ROS) ↑ ROS Driver Upstream cytotoxic trigger Primary studies show TQ rapidly increases ROS; antioxidant/ROS modulation attenuates downstream effects, supporting ROS as an initiating mechanism in multiple cancer contexts (ref)
2 Glutathione (GSH) redox buffering ↓ GSH Driver Redox-collapse amplification Same prostate cancer study reports early GSH depletion alongside ROS rise; together these form a redox “one-two punch” that helps explain selective stress in tumor cells (ref)
3 Mitochondrial integrity (ΔΨm) ↓ ΔΨm Driver Mitochondrial dysfunction (MOMP axis) Primary leukemia/cancer study reports disruption of mitochondrial membrane potential after TQ exposure (mitochondrial events central to TQ-mediated death) (ref)
4 Intrinsic apoptosis (caspase-9 → caspase-3; PARP) ↑ caspases / ↑ apoptosis Driver Execution-phase cell death Same primary paper reports activation of caspases (8/9/3) with mitochondrial involvement—core evidence for apoptosis as the major outcome pathway (ref)
5 NF-κB signaling ↓ NF-κB activity Secondary Reduced pro-survival / inflammatory transcription Colon cancer work: TQ induces cell death and chemosensitizes cells by inhibiting NF-κB signaling (explicit pathway-direction support) (ref)
6 STAT3 signaling ↓ p-STAT3 / ↓ STAT3 activation Secondary Reduced survival/proliferation signaling Gastric cancer study explicitly reports TQ suppresses constitutive STAT3 activation and related signaling readouts (ref)
7 NRF2 antioxidant-response axis (NRF2/HO-1 program) ↑ NRF2 pathway (often as stress-response) Adaptive Cellular antioxidant counter-response In TNBC context, a primary study reports TQ upregulates NRF2 (and evaluates downstream immune/checkpoint consequences), consistent with NRF2 acting as an adaptive response to redox stress (ref)
8 HIF-1α hypoxia signaling ↓ HIF-1α protein / ↓ HIF-1α program Adaptive Loss of hypoxia survival signaling Renal cancer hypoxia paper identifies TQ as suppressing HIF-1α and links this to selective killing under hypoxia (ref)
9 Glycolysis / Warburg output (hypoxia-linked) ↓ glycolysis (↓ HIF-1α–mediated glycolytic genes; ↓ glycolytic metabolism) Phenotypic Metabolic suppression In hypoxic renal cancer, TQ suppresses HIF-1α–mediated glycolysis; in CRC, TQ inhibits glycolytic metabolism alongside tumor growth limitation (ref)  |  (ref)


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⟱
4670- RES,  CUR,  EGCG,  TQ,    Targeting aging pathways with natural compounds: a review of curcumin, epigallocatechin gallate, thymoquinone, and resveratrol
- Review, Nor, NA
*antiOx↑, *Inflam↓, *AntiAge↑, *SIRT1↑, *SIRT3↑, *FOXO↑, *ROS↓,
3407- TQ,    Thymoquinone and its pharmacological perspective: A review
- Review, NA, NA
*antiOx↑, *ROS↓, *GSTs↑, *GSR↑, *GSH↑, *RenoP↑, *IL1β↓, *TNF-α↓, *MMP13↓, *COX2↓, *PGE2↓, *radioP↑, Twist↓, EMT↓, NF-kB↓, p‑PI3K↓, p‑Akt↓, p‑GSK‐3β↓, DNMT1↓, HDAC↓,
3409- TQ,    Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives
- in-vivo, Nor, NA
*MDA↓, *TGF-β↓, *CRP↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *Casp3↓, *GSH↑, *NRF2↑, *IL10↑, *neuroP↑, *ROS↓, *Apoptosis↓, *Inflam↓,
3410- TQ,    Anti-inflammatory effects of thymoquinone and its protective effects against several diseases
- Review, Arthritis, NA
*Inflam↓, *antiOx↑, *COX2↓, *NRF2↑, *HO-1↑, *IL1β↓, *IL6↓, *TNF-α↓, *IFN-γ↓, *PGE2↓, *cardioP↑, *Catalase↑, *SOD↑, *Thiols↑, *neuroP↑, *IL12↓, *MCP1↓, *CXCc↓, *ROS↓,
3415- TQ,    ROS%20was%20induced,TQ%20in%20SCLC%20cell%20lines">The anti-neoplastic impact of thymoquinone from Nigella sativa on small cell lung cancer: In vitro and in vivo investigations
- in-vitro, Lung, H446
tumCV↓, TumCCA↑, ROS↓, CycB/CCNB1↑, CycD3↑, cycA1/CCNA1↓, cycE/CCNE↓, cDC2↓, antiOx↑, PARP↓, NRF2↓, ARE/EpRE↑, eff↑,
3404- TQ,    The Neuroprotective Effects of Thymoquinone: A Review
- Review, Var, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, AntiCan↑, *TNF-α↓, *IL6↓, *IL1β↓, *NF-kB↓, *iNOS↓, *NRF2↑, *neuroP↑, *MMP↑, *ROS↓, *MDA↓, *GSH↑, *Catalase↑, *SOD↑, *IL12↓, *MCP1↓, *IP-10/CXCL-10↓, *PGE2↓,
3418- TQ,    Thymoquinone suppresses metastasis of melanoma cells by inhibition of NLRP3 inflammasome
- in-vitro, Melanoma, A375 - in-vivo, NA, NA
TumMeta↓, TumCMig↓, NLRP3↓, Casp1↓, IL1β↓, IL18↓, ROS↓, NF-kB↓,
3420- TQ,    Thymoquinone alleviates the accumulation of ROS and pyroptosis and promotes perforator skin flap survival through SIRT1/NF-κB pathway
- in-vitro, Nor, HUVECs - in-vitro, NA, NA
*NF-kB↓, *NLRP3↓, *angioG↑, *MMP9↑, *VEGF↑, *OS↑, *Pyro?, *ROS↓, *Apoptosis↓, *SIRT1↑, *SOD1↑, *HO-1↑, *eNOS↑, *ASC?, *Casp1↓, *IL1β↓, *IL18↓,
3405- TQ,  doxoR,    Protective effect of thymoquinone against doxorubicin-induced cardiotoxicity and the underlying mechanism
- vitro+vivo, NA, NA
*cardioP↑, *NRF2↑, *HO-1↑, *ROS↓, *NQO1↑, *COX2↓, *NOX4↓, *GPx4↑, *FTH1↑, *p‑mTOR↓, *TGF-β↓,
3401- TQ,    Molecular mechanisms and signaling pathways of black cumin (Nigella sativa) and its active constituent, thymoquinone: a review
- Review, Var, NA
TumCP↓, *antiOx↑, *ROS↓, NRF2↑, NF-kB↓, TumCCA↑, *GABA↑, P53↑, P21↑, AMPK↑, neuroP↑, cardioP↑, hepatoP↑,
3399- TQ,    Anticancer Effects of Thymoquinone through the Antioxidant Activity, Upregulation of Nrf2, and Downregulation of PD-L1 in Triple-Negative Breast Cancer Cells
- in-vitro, BC, MDA-MB-231 - NA, BC, MDA-MB-468
ROS↓, H2O2↓, Catalase↑, SOD↑, GSH↑, NQO1↑, GCLM↑, NRF2↑, PD-L1↓, GSSG↑, GPx1⇅, GPx4↓,
3398- TQ,  5-FU,    Impact of thymoquinone on the Nrf2/HO-1 and MAPK/NF-κB axis in mitigating 5-fluorouracil-induced acute kidney injury in vivo
- in-vivo, Nor, NA
*RenoP↑, *TAC↑, *ROS↓, *lipid-P↓, *p38↓, *MAPK↓, *NF-kB↓, *NRF2↑, *HO-1↑, *MDA↓, *GPx↑, *GSR↑, *Catalase↑, *BUN↓, *LDH↓, *IL1β↓,
2136- TQ,    Nigella sativa and thymoquinone suppress cyclooxygenase-2 and oxidative stress in pancreatic tissue of streptozotocin-induced diabetic rats
- in-vivo, Nor, NA
*COX2↓, *lipid-P↓, *SOD↑, *ROS↓, *Inflam↓, *NF-kB↓,
3564- TQ,    The Potential Neuroprotective Effect of Thymoquinone on Scopolamine-Induced In Vivo Alzheimer's Disease-like Condition: Mechanistic Insights
- in-vivo, AD, NA
*Inflam↓, *AntiCan↑, *antiOx↑, *neuroP↑, *cognitive↑, *Aβ↓, *PPARγ↑, *NF-kB↓, *p‑tau↓, *MMP↑, *memory↑, *NF-kB↓, *ROS↓,
3565- TQ,    Thymoquinone as a potential therapeutic for Alzheimer’s disease in transgenic Drosophila melanogaster model
*cognitive↑, *ROS↓, *SOD↑, *AChE↝, *Aβ↓,
3571- TQ,    The Role of Thymoquinone in Inflammatory Response in Chronic Diseases
- Review, Var, NA - Review, Stroke, NA
*BioAv↓, *BioAv↑, *Inflam↓, *antiOx↑, *ROS↓, *GSH↑, *GSTs↑, *MPO↓, *NF-kB↓, *COX2↓, *IL1β↓, *TNF-α↓, *IFN-γ↓, *IL6↓, *cardioP↑, *lipid-P↓, *TAC↑, *RenoP↑, Apoptosis↑, TumCCA↑, TumCP↓, TumCMig↓, angioG↓, TNF-α↓, NF-kB↓, ROS↑, EMT↓, *Aβ↓, *p‑tau↓, *BACE↓, *TLR2↓, *TLR4↓, *MyD88↓, *IRF3↓, *eff↑, eff↑, DNAdam↑, *iNOS↓,
4172- TQ,    Chronic Administration of Thymoquinone Enhances Adult Hippocampal Neurogenesis and Improves Memory in Rats Via Regulating the BDNF Signaling Pathway
- in-vivo, AD, NA
*cognitive↑, *BDNF↑, *p‑CREB↑, *ROS↓, *memory↑,
4538- TQ,    Thymoquinone Anticancer Effects Through the Upregulation of NRF2 and the Downregulation of PD‐L1 in MDA‐MB‐231 Triple‐Negative Breast Cancer Cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
antiOx↑, H2O2↓, Catalase↑, SOD↑, GSH↑, PRNP↑, NQO1↑, GCLM↑, NRF2↑, PD-L1↓, chemoPv↑, ROS↓,
5024- TQ,    Thymoquinone: A Tie-Breaker in SARS-CoV2-Infected Cancer Patients?
- Review, Covid, NA
*NRF2↑, *NF-kB↓, *Inflam↓, *ROS↓, *HO-1↑, antiOx↑, GSH↑, GSTs↑, GSR↑, SOD1↑, Catalase↑, GPx↑, p62↓, Beclin-1↑, Sepsis↓, cardioP↑, hepatoP↑, neuroP↑,
3559- TQ,    Molecular signaling pathway targeted therapeutic potential of thymoquinone in Alzheimer’s disease
- Review, AD, NA - Review, Var, NA
*antiOx↑, *Inflam↓, *AChE↓, AntiCan↑, *cardioP↑, *RenoP↑, *neuroP↑, *hepatoP↑, TumCG↓, Apoptosis↑, PI3K↓, Akt↑, TumCCA↑, angioG↓, *NF-kB↓, *TLR2↓, *TLR4↓, *MyD88↓, *TRIF↓, *IRF3↓, *IL1β↓, *IL6↓, *IL12↓, *NRF2↑, *COX2↓, *VEGF↓, *MMP9↓, *cMyc↓, *cycD1/CCND1↓, *TumCP↓, *TumCI↓, *MDA↓, *TGF-β↓, *CRP↓, *Casp3↓, *GSH↑, *IL10↑, *iNOS↑, *lipid-P↓, *SOD↑, *H2O2↓, *ROS↓, *LDH↓, *Catalase↑, *GPx↑, *AChE↓, *cognitive↑, *MAPK↑, *JNK↑, *BAX↓, *memory↑, *Aβ↓, *MMP↑,
3554- TQ,    Neuroprotective efficacy of thymoquinone against amyloid beta-induced neurotoxicity in human induced pluripotent stem cell-derived cholinergic neurons
- in-vitro, AD, NA
*GSH↑, *ROS↓, *neuroP↑, *Casp3↓, *Casp7↓, *antiOx↓, *H2O2↓,
3432- TQ,    Thymoquinone: Review of Its Potential in the Treatment of Neurological Diseases
- Review, AD, NA - Review, Park, NA
*memory↑, *cognitive↑, *ROS↓, *Inflam↓, *antiOx↑, *TLR1↓, *AChE↓, *MMP↑, *neuroP↑, *lipid-P↓, *SOD↑, *GSH↑, *Ach↑,
2134- TQ,    Modulation of Nrf2/HO1 Pathway by Thymoquinone to Exert Protection Against Diazinon-induced Myocardial Infarction in Rats
- in-vivo, Nor, NA
*ALAT↓, *AST↓, *MDA↓, *ROS↓, *GSSG↓, *GSH↑, *VitE↑, *VitC↑, *NRF2↑, *HO-1↑, *NQO1↑, *SOD↑, *cardioP↑, *GSH/GSSG↑, *GPx↑,
2092- TQ,    Dissecting the Potential Roles of Nigella sativa and Its Constituent Thymoquinone on the Prevention and on the Progression of Alzheimer's Disease
- Review, AD, NA
*iNOS↓, *ROS↓, *GSH↑, *neuroP↑, *MMPs↓, *MMP↑, *TXNIP↓, *Prx↑, *memory↑, *MDA↓, *SOD↑, *Catalase↑, *BioAv↑,
2084- TQ,    Thymoquinone, as an anticancer molecule: from basic research to clinical investigation
- Review, Var, NA
*ROS↓, *chemoPv↑, ROS↑, ROS⇅, MUC4↓, selectivity↑, AR↓, cycD1/CCND1↓, Bcl-2↓, Bcl-xL↓, survivin↓, Mcl-1↓, VEGF↓, cl‑PARP↑, ROS↑, HSP70/HSPA5↑, P53↑, miR-34a↑, Rac1↓, TumCCA↑, NOTCH↓, NF-kB↓, IκB↓, p‑p65↓, IAP1↓, IAP2↑, XIAP↓, TNF-α↓, COX2↓, Inflam↓, α-tubulin↓, Twist↓, EMT↓, mTOR↓, PI3K↓, Akt↓, BioAv↓, ChemoSen↑, BioAv↑, PTEN↑, chemoPv↑, RadioS↑, *Half-Life↝, *BioAv↝,
2088- TQ,    Nigella sativa L. and Its Bioactive Constituents as Hepatoprotectant: A Review
- Review, Nor, NA
*hepatoP↑, *lipid-P↓, *Thiols↑, *ROS↓, *Catalase↑, *SOD↑, *GSTs↑, *NF-kB↓, *COX2↓, *LOX1↓,
2089- TQ,    Modulation of Hydrogen Peroxide-Induced Oxidative Stress in Human Neuronal Cells by Thymoquinone-Rich Fraction and Thymoquinone via Transcriptomic Regulation of Antioxidant and Apoptotic Signaling Genes
- in-vitro, Nor, SH-SY5Y
*neuroP↑, *ROS↓, *SOD1↑, *Catalase↑,
2094- TQ,    Cytotoxicity of Nigella sativa Extracts Against Cancer Cells: A Review of In Vitro and In Vivo Studies
- Review, Var, NA
ROS↑, angioG↓, TumMeta↓, VEGF↓, MMPs↓, P53↑, BAX↑, Casp↑, Bcl-2↓, survivin↓, *ROS↓, ChemoSen↑, chemoP↑, MDR1↓, BioAv↓, BioAv↑,
1935- TQ,    Potential anticancer properties and mechanisms of thymoquinone in osteosarcoma and bone metastasis
- Review, OS, NA
Apoptosis↑, TumCCA↑, angioG↓, TumMeta↓, ROS↑, P53↑, Twist↓, E-cadherin↑, N-cadherin↓, NF-kB↓, IL8↓, XIAP↓, Bcl-2↓, STAT3↓, MAPK↓, PI3K↓, Akt↓, ERK↓, MMP2↓, MMP9↓, *ROS↓, HO-1↑, selectivity↑, TumCG↓,
1937- TQ,    Migration and Proliferation Effects of Thymoquinone-Loaded Nanostructured Lipid Carrier (TQ-NLC) and Thymoquinone (TQ) on In Vitro Wound Healing Models
- NA, Nor, 3T3
*ROS↓, *antiOx↓, *BioAv↓, *BioAv↑, *NO↑, *SOD↑, *GPx↑, *Catalase↑,
2118- TQ,  Rad,    In vivo radioprotective effects of Nigella sativa L oil and reduced glutathione against irradiation-induced oxidative injury and number of peripheral blood lymphocytes in rats
- in-vivo, Nor, NA
*ROS↓, RenoP↑, hepatoP↑,
2119- TQ,    Dual properties of Nigella Sativa: anti-oxidant and pro-oxidant
- Review, Var, NA
*ROS↓, ROS↑, chemoP↑, RenoP↑, hepatoP↑, NLRP3↓, neuroP↑, NF-kB↓, P21↑, HDAC↓, Apoptosis↑, TumCP↓, GSH↓, GADD45A↑, GSK‐3β↑,
2122- TQ,    Review on Molecular and Therapeutic Potential of Thymoquinone in Cancer
- Review, Var, NA
ChemoSen↓, *ROS↓, *GSH↑, RenoP↑, hepatoP↑, COX2↓, NF-kB↓, chemoPv↑, neuroP↑, TumCCA↑, P21↑, p27↑, ROS↑, DNAdam↑, MUC4↓,
2117- TQ,    Effects of Nigella sativa L. on Lipid Peroxidation and Reduced Glutathione Levels in Erythrocytes of Broiler Chickens
- in-vivo, Nor, NA
*GSH↑, *ROS↓,
2130- TQ,    Thymoquinone Attenuates Brain Injury via an Anti-oxidative Pathway in a Status Epilepticus Rat Model
- in-vivo, Nor, NA
*eff↑, *memory↑, *NRF2↑, *HO-1↑, *SOD↑, *ROS↓,
2131- TQ,    Therapeutic impact of thymoquninone to alleviate ischemic brain injury via Nrf2/HO-1 pathway
- in-vitro, Stroke, NA - in-vivo, Nor, NA
*eff↑, *OS↑, *Inflam↓, *ROS↓, *NRF2↑, *HO-1↑,
2106- TQ,    Cancer: Thymoquinone antioxidant/pro-oxidant effect as potential anticancer remedy
- Review, Var, NA
Apoptosis↑, TumCCA↑, ROS↑, *Catalase↑, *SOD↑, *GR↑, *GSTA1↓, *GPx↑, *H2O2↓, *ROS↓, *lipid-P↓, *HO-1↑, p‑Akt↓, AMPKα↑, NK cell↑, selectivity↑, Dose↝, eff↑, GSH↓, eff↓, P53↑, p‑STAT3↓, PI3K↑, MAPK↑, GSK‐3β↑, ChemoSen↑, RadioS↑, BioAv↓, NRF2↑,
2113- TQ,    Potential role of Nigella sativa (NS) in abating oxidative stress-induced toxicity in rats: a possible protection mechanism
- in-vivo, Nor, NA
*antiOx↑, *RenoP↑, *hepatoP↑, *SOD↑, *GSH↑, *ROS↓, *lipid-P↓, ALAT↓, creat↓,
2116- TQ,  Cisplatin,    Oral administration of Nigella sativa oil ameliorates the effect of cisplatin on membrane enzymes, carbohydrate metabolism and oxidative damage in rat liver
- in-vivo, Nor, NA
*hepatoP↑, *antiOx↑, *ROS↓, ALAT↓, AST↓,

Showing Research Papers: 1 to 39 of 39

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 39

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   ARE/EpRE↑, 1,   Catalase↑, 3,   GCLM↑, 2,   GPx↑, 1,   GPx1⇅, 1,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 3,   GSR↑, 1,   GSSG↑, 1,   GSTs↑, 1,   H2O2↓, 2,   HO-1↑, 1,   NQO1↑, 2,   NRF2↓, 1,   NRF2↑, 4,   ROS↓, 4,   ROS↑, 8,   ROS⇅, 1,   SOD↑, 2,   SOD1↑, 1,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2,   AMPK↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Akt↑, 1,   p‑Akt↓, 2,   Apoptosis↑, 5,   BAX↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 1,   Casp↑, 1,   Casp1↓, 1,   IAP1↓, 1,   IAP2↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p27↑, 1,   survivin↓, 2,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   p62↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   DNMT1↓, 1,   GADD45A↑, 1,   P53↑, 5,   PARP↓, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 1,   CycD3↑, 1,   cycE/CCNE↓, 1,   P21↑, 3,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State ⓘ

cDC2↓, 1,   EMT↓, 3,   ERK↓, 1,   GSK‐3β↑, 2,   p‑GSK‐3β↓, 1,   HDAC↓, 2,   miR-34a↑, 1,   mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 3,   PI3K↑, 1,   p‑PI3K↓, 1,   PTEN↑, 1,   STAT3↓, 1,   p‑STAT3↓, 1,   TumCG↓, 2,  

Migration ⓘ

E-cadherin↑, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   MUC4↓, 2,   N-cadherin↓, 1,   PRNP↑, 1,   Rac1↓, 1,   TumCMig↓, 2,   TumCP↓, 3,   TumMeta↓, 3,   Twist↓, 3,   α-tubulin↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL18↓, 1,   IL1β↓, 1,   IL8↓, 1,   Inflam↓, 1,   IκB↓, 1,   NF-kB↓, 8,   NK cell↑, 1,   p‑p65↓, 1,   PD-L1↓, 2,   TNF-α↓, 2,  

Protein Aggregation ⓘ

NLRP3↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 2,   ChemoSen↓, 1,   ChemoSen↑, 3,   Dose↝, 1,   eff↓, 1,   eff↑, 3,   MDR1↓, 1,   RadioS↑, 2,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   AR↓, 1,   AST↓, 1,   creat↓, 1,   PD-L1↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 2,   cardioP↑, 2,   chemoP↑, 2,   chemoPv↑, 3,   hepatoP↑, 5,   neuroP↑, 4,   RenoP↑, 3,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 126

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 2,   antiOx↑, 10,   Catalase↑, 9,   GPx↑, 5,   GPx4↑, 1,   GSH↑, 12,   GSH/GSSG↑, 1,   GSR↑, 2,   GSSG↓, 1,   GSTA1↓, 1,   GSTs↑, 3,   H2O2↓, 3,   HO-1↑, 9,   lipid-P↓, 8,   MDA↓, 6,   MPO↓, 1,   NOX4↓, 1,   NQO1↑, 2,   NRF2↑, 10,   Prx↑, 1,   ROS↓, 35,   SIRT3↑, 1,   SOD↑, 13,   SOD1↑, 2,   TAC↑, 2,   Thiols↑, 2,   VitC↑, 1,   VitE↑, 1,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 5,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   BUN↓, 1,   cMyc↓, 1,   p‑CREB↑, 1,   LDH↓, 2,   PPARγ↑, 1,   SIRT1↑, 2,  

Cell Death ⓘ

Apoptosis↓, 2,   BAX↓, 1,   Casp1↓, 1,   Casp3↓, 3,   Casp7↓, 1,   iNOS↓, 3,   iNOS↑, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   p38↓, 1,   Pyro?, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

FOXO↑, 1,   p‑mTOR↓, 1,  

Migration ⓘ

MMP13↓, 1,   MMP9↓, 1,   MMP9↑, 1,   MMPs↓, 1,   TGF-β↓, 3,   TumCI↓, 1,   TumCP↓, 1,   TXNIP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   eNOS↑, 1,   LOX1↓, 1,   NO↑, 1,   VEGF↓, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

ASC?, 1,   COX2↓, 7,   CRP↓, 2,   CXCc↓, 1,   IFN-γ↓, 2,   IL10↑, 2,   IL12↓, 3,   IL18↓, 1,   IL1β↓, 8,   IL6↓, 4,   Inflam↓, 11,   IP-10/CXCL-10↓, 1,   MCP1↓, 2,   MyD88↓, 2,   NF-kB↓, 11,   PGE2↓, 3,   TLR1↓, 1,   TLR2↓, 2,   TLR4↓, 2,   TNF-α↓, 5,   TRIF↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 3,   AChE↝, 1,   BDNF↑, 1,   GABA↑, 1,   p‑tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 4,   BACE↓, 1,   NLRP3↓, 1,  

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 3,   BioAv↝, 1,   eff↑, 3,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   CRP↓, 2,   IL6↓, 4,   LDH↓, 2,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   cardioP↑, 5,   chemoPv↑, 1,   cognitive↑, 5,   hepatoP↑, 4,   memory↑, 6,   neuroP↑, 9,   OS↑, 2,   radioP↑, 1,   RenoP↑, 5,  

Infection & Microbiome ⓘ

IRF3↓, 2,  
Total Targets: 119

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
39 Thymoquinone
1 Resveratrol
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 doxorubicin
1 5-fluorouracil
1 Radiotherapy/Radiation
1 Cisplatin
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#:162  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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