Thymoquinone / mTOR 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↓, 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)


mTOR, mammalian target of rapamycin: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
mTOR (mechanistic target of rapamycin) is a central regulator of cell growth, proliferation, metabolism, and survival. It is a serine/threonine kinase that integrates signals from nutrients, growth factors, and cellular energy status.
mTOR promotes protein synthesis and cell growth by activating downstream targets such as S6 kinase and 4E-BP1. In cancer, this pathway can become hyperactivated, leading to uncontrolled cell proliferation.

mTor Inhibitors:
-rapamycin (Sirolimus): classic natural product mTOR inhibitor
-Curcumin
-Resveratrol
-Epigallocatechin Gallate (EGCG)
-Honokiol
Scientific Papers found: Click to Expand⟱
4774- 5-FU,  TQ,  CoQ10,    Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation
- in-vitro, CRC, NA
AntiCan↑, TumCCA↑, Apoptosis↑, eff↑, Bcl-2↓, survivin↓, P21↑, p27↑, BAX↑, Cyt‑c↑, Casp3↑, PI3K↓, Akt↓, mTOR↓, Hif1a↓, PTEN↑, AMPKα↑, PDH↑, LDHA↓, antiOx↓, ROS↑, AntiCan↑,
3411- TQ,    Anticancer and Anti-Metastatic Role of Thymoquinone: Regulation of Oncogenic Signaling Cascades by Thymoquinone
- Review, Var, NA
p‑STAT3↓, cycD1/CCND1↓, JAK2↓, β-catenin/ZEB1↓, cMyc↓, MMP7↓, MET↓, p‑Akt↓, p‑mTOR↓, CXCR4↓, Bcl-2↓, BAX↑, ROS↑, Cyt‑c↑, Twist↓, Zeb1↓, E-cadherin↑, p‑p38↑, p‑MAPK↑, ERK↑, eff↑, ERK↓, TumCP↓, TumCMig↓, TumCI↓,
3422- TQ,    Thymoquinone, as a Novel Therapeutic Candidate of Cancers
- Review, Var, NA
selectivity↑, P53↑, PTEN↑, NF-kB↓, PPARγ↓, cMyc↓, Casp↑, *BioAv↓, BioAv↝, eff↑, survivin↓, Bcl-xL↓, Bcl-2↓, Akt↓, BAX↑, cl‑PARP↑, CXCR4↓, MMP9↓, VEGFR2↓, Ki-67↓, COX2↓, JAK2↓, cSrc↓, Apoptosis↑, p‑STAT3↓, cycD1/CCND1↓, Casp3↑, Casp7↑, Casp9↑, N-cadherin↓, Vim↓, Twist↓, E-cadherin↑, ChemoSen↑, eff↑, EMT↓, ROS↑, DNMT1↓, eff↑, EZH2↓, hepatoP↑, Zeb1↓, RadioS↑, HDAC↓, HDAC1↓, HDAC2↓, HDAC3↓, *NAD↑, *SIRT1↑, SIRT1↓, *Inflam↓, *CRP↓, *TNF-α↓, *IL6↓, *IL1β↓, *eff↑, *MDA↓, *NO↓, *GSH↑, *SOD↑, *Catalase↑, *GPx↑, PI3K↓, mTOR↓,
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↓,
3397- TQ,    Thymoquinone: A Promising Therapeutic Agent for the Treatment of Colorectal Cancer
- Review, CRC, NA
ChemoSen↑, *Half-Life↝, *BioAv↝, *antiOx↑, *Inflam↓, *hepatoP↑, TumCP↓, TumCCA↑, Apoptosis↑, angioG↑, selectivity↑, JNK↑, p38↑, p‑NF-kB↑, ERK↓, PI3K↓, PTEN↑, Akt↓, mTOR↓, EMT↓, Twist↓, E-cadherin↓, ROS⇅, *Catalase↑, *SOD↑, *GSTA1↑, *GPx↑, *PGE2↓, *IL1β↓, *COX2↓, *MMP13↓, MMPs↓, TumMeta↓, VEGF↓, STAT3↓, BAX↑, Bcl-2↑, Casp9↑, Casp7↑, Casp3↑, cl‑PARP↑, survivin↓, cMyc↓, cycD1/CCND1↓, p27↑, P21↑, GSK‐3β↓, β-catenin/ZEB1↓, chemoP↑,
3427- TQ,    Chemopreventive and Anticancer Effects of Thymoquinone: Cellular and Molecular Targets
ROS⇅, Fas↑, DR5↑, TRAIL↑, Casp3↑, Casp8↑, Casp9↑, P53↑, mTOR↓, Bcl-2↓, BID↓, CXCR4↓, JNK↑, p38↑, MAPK↑, LC3II↑, ATG7↑, Beclin-1↑, AMPK↑, PPARγ↑, eIF2α↓, P70S6K↓, VEGF↓, ERK↓, NF-kB↓, XIAP↓, survivin↓, p65↓, DLC1↑, FOXO↑, TET2↑, CYP1B1↑, UHRF1↓, DNMT1↓, HDAC1↓, IL2↑, IL1↓, IL6↓, IL10↓, IL12↓, TNF-α↓, iNOS↓, COX2↓, 5LO↓, AP-1↓, PI3K↓, Akt↓, cMET↓, VEGFR2↓, CXCL1↓, ITGA5↓, Wnt↓, β-catenin/ZEB1↓, GSK‐3β↓, Myc↓, cycD1/CCND1↓, N-cadherin↓, Snail↓, Slug↓, Vim↓, Twist↓, Zeb1↓, MMP2↓, MMP7↓, MMP9↓, JAK2↓, STAT3↓, NOTCH↓, cycA1/CCNA1↓, CDK2↓, CDK4↓, CDK6↓, CDC2↓, CDC25↓, Mcl-1↓, E2Fs↓, p16↑, p27↑, P21↑, ChemoSen↑,
3425- TQ,    Advances in research on the relationship between thymoquinone and pancreatic cancer
Apoptosis↑, TumCP↓, TumCI↓, TumMeta↓, ChemoSen↑, angioG↓, Inflam↓, NF-kB↓, PI3K↓, Akt↓, TGF-β↓, Jun↓, p38↑, MAPK↑, MMP9↓, PKM2↓, ROS↑, JNK↑, MUC4↓, TGF-β↑, Dose↝, FAK↓, NOTCH↓, PTEN↑, mTOR↓, Warburg↓, XIAP↓, COX2↓, Casp9↑, Ki-67↓, CD34↓, VEGF↓, MCP1↓, survivin↓, Cyt‑c↑, Casp3↑, H4↑, HDAC↓,
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↝,
2127- TQ,    Therapeutic Potential of Thymoquinone in Glioblastoma Treatment: Targeting Major Gliomagenesis Signaling Pathways
- Review, GBM, NA
chemoP↑, ChemoSen↑, BioAv↑, PTEN↑, PI3K↓, Akt↓, TumCCA↓, NF-kB↓, p‑Akt↓, p65↓, XIAP↓, Bcl-2↓, COX2↓, VEGF↓, mTOR↓, RAS↓, Raf↓, MEK↓, ERK↓, MMP2↓, MMP9↓, TumCMig↓, TumCI↓, Casp↑, cl‑PARP↑, ROS⇅, ROS↑, MMP↓, eff↑, Telomerase↓, DNAdam↑, Apoptosis↑, STAT3↓, RadioS↑,

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   ROS↑, 7,   ROS⇅, 4,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   CDC25↓, 1,   MEK↓, 1,   MMP↓, 1,   Raf↓, 1,   XIAP↓, 4,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   ATG7↑, 1,   cMyc↓, 3,   LDHA↓, 1,   PDH↑, 1,   PKM2↓, 1,   PPARγ↓, 1,   PPARγ↑, 1,   SIRT1↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 7,   p‑Akt↓, 2,   Apoptosis↑, 5,   BAX↑, 4,   Bcl-2↓, 6,   Bcl-2↑, 1,   Bcl-xL↓, 2,   BID↓, 1,   Casp↑, 2,   Casp3↑, 5,   Casp7↑, 2,   Casp8↑, 1,   Casp9↑, 4,   Cyt‑c↑, 3,   DR5↑, 1,   Fas↑, 1,   IAP1↓, 1,   IAP2↑, 1,   iNOS↓, 1,   JNK↑, 3,   MAPK↑, 2,   p‑MAPK↑, 1,   Mcl-1↓, 2,   Myc↓, 1,   p27↑, 3,   p38↑, 3,   p‑p38↑, 1,   survivin↓, 6,   Telomerase↓, 1,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,   cSrc↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   H4↑, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↓, 1,   HSP70/HSPA5↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

CYP1B1↑, 1,   DNAdam↑, 1,   DNMT1↓, 2,   p16↑, 1,   P53↑, 3,   cl‑PARP↑, 4,   UHRF1↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 5,   E2Fs↓, 1,   P21↑, 3,   TumCCA↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   cMET↓, 1,   EMT↓, 3,   ERK↓, 4,   ERK↑, 1,   FOXO↑, 1,   GSK‐3β↓, 2,   HDAC↓, 2,   HDAC1↓, 2,   HDAC2↓, 1,   HDAC3↓, 1,   Jun↓, 1,   miR-34a↑, 1,   mTOR↓, 7,   p‑mTOR↓, 1,   NOTCH↓, 3,   P70S6K↓, 1,   PI3K↓, 7,   PTEN↑, 6,   RAS↓, 1,   STAT3↓, 3,   p‑STAT3↓, 2,   Wnt↓, 1,  

Migration ⓘ

5LO↓, 1,   AP-1↓, 1,   DLC1↑, 1,   E-cadherin↓, 1,   E-cadherin↑, 2,   FAK↓, 1,   ITGA5↓, 1,   Ki-67↓, 2,   MET↓, 1,   MMP2↓, 2,   MMP7↓, 2,   MMP9↓, 4,   MMPs↓, 1,   MUC4↓, 2,   N-cadherin↓, 2,   Rac1↓, 1,   Slug↓, 1,   Snail↓, 1,   TGF-β↓, 1,   TGF-β↑, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 3,   TumMeta↓, 2,   Twist↓, 5,   Vim↓, 2,   Zeb1↓, 3,   α-tubulin↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   angioG↑, 1,   Hif1a↓, 1,   VEGF↓, 5,   VEGFR2↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 5,   CXCL1↓, 1,   CXCR4↓, 3,   IL1↓, 1,   IL10↓, 1,   IL12↓, 1,   IL2↑, 1,   IL6↓, 1,   Inflam↓, 2,   IκB↓, 1,   JAK2↓, 3,   MCP1↓, 1,   NF-kB↓, 5,   p‑NF-kB↑, 1,   p65↓, 2,   p‑p65↓, 1,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 6,   Dose↝, 1,   eff↑, 6,   RadioS↑, 3,   selectivity↑, 3,   TET2↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   EZH2↓, 1,   IL6↓, 1,   Ki-67↓, 2,   Myc↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   chemoP↑, 2,   chemoPv↑, 1,   hepatoP↑, 1,  
Total Targets: 166

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 2,   GPx↑, 2,   GPx4↑, 1,   GSH↑, 1,   GSTA1↑, 1,   HO-1↑, 1,   MDA↓, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 2,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,  

Core Metabolism/Glycolysis ⓘ

NAD↑, 1,   SIRT1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑mTOR↓, 1,  

Migration ⓘ

MMP13↓, 1,   TGF-β↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CRP↓, 1,   IL1β↓, 2,   IL6↓, 1,   Inflam↓, 2,   PGE2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

CRP↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoPv↑, 1,   hepatoP↑, 1,  
Total Targets: 36

Scientific Paper Hit Count for: mTOR, mammalian target of rapamycin
9 Thymoquinone
1 5-fluorouracil
1 Coenzyme Q10
1 doxorubicin
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#:209  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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