Thymoquinone / TGF-β 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)


TGF-β, transforming growth factor-beta: Click to Expand ⟱
Source: HalifaxProj(inhibit) CGL-CS TCGA
Type:
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses.
Anti-inflammatory cytokine.
In normal tissues, TGF-β plays an essential role in cell cycle regulation, immune function, and tissue remodeling.
- In early carcinogenesis, TGF-β typically acts as a tumor suppressor by inhibiting cell proliferation and inducing apoptosis.

In advanced cancers, cells frequently become resistant to the growth-inhibitory effects of TGF-β.
- TGF-β then switches roles and promotes tumor progression by stimulating epithelial-to-mesenchymal transition (EMT), cell invasion, metastasis, and immune evasion.

Non-canonical (Smad-independent) pathways, such as MAPK, PI3K/Akt, and Rho signaling, also contribute to TGF-β-mediated responses.

Elevated levels of TGF-β have been detected in many advanced-stage cancers, including breast, lung, colorectal, pancreatic, and prostate cancers.
 - The switch from a tumor-suppressive to a tumor-promoting role is often associated with increased TGF-β production and activation in the tumor microenvironment.

High TGF-β expression or signaling activity is frequently correlated with aggressive disease features, resistance to therapy, increased metastasis, and poorer overall survival in many cancer types.
Scientific Papers found: Click to Expand⟱
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↓,
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↓,
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↑,
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↓,
1138- TQ,    Thymoquinone inhibits epithelial-mesenchymal transition in prostate cancer cells by negatively regulating the TGF-β/Smad2/3 signaling pathway
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
TumMeta↓, EMT↓, E-cadherin↑, Vim↓, Slug↓, TGF-β↓, SMAD2↓, SMAD3↓,
2132- TQ,    Thymoquinone treatment modulates the Nrf2/HO-1 signaling pathway and abrogates the inflammatory response in an animal model of lung fibrosis
- in-vivo, Nor, NA
*Weight∅, *antiOx↑, *lipid-P↓, *MMP7↓, *Casp3↓, *BAX↓, *TGF-β↓, *Diff↑, *NRF2↓, *HO-1↓, *NF-kB↓, *IκB↑,

Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

PKM2↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↑, 2,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   JNK↑, 1,   MAPK↑, 1,   p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

H4↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   EMT↓, 1,   HDAC↓, 1,   Jun↓, 1,   mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 2,   PTEN↑, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   FAK↓, 1,   Ki-67↓, 1,   MMP9↓, 1,   MUC4↓, 1,   Slug↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   TGF-β↓, 2,   TGF-β↑, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 2,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,   MCP1↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↝, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 49

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx↑, 1,   GPx4↑, 1,   GSH↑, 2,   H2O2↓, 1,   HO-1↓, 1,   HO-1↑, 1,   lipid-P↓, 2,   MDA↓, 2,   NOX4↓, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 3,   ROS↓, 3,   SOD↑, 1,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   LDH↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   BAX↓, 2,   Casp3↓, 3,   iNOS↑, 1,   JNK↑, 1,   MAPK↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   p‑mTOR↓, 1,  

Migration ⓘ

MMP7↓, 1,   MMP9↓, 1,   TGF-β↓, 4,   TumCI↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CRP↓, 2,   IL10↑, 2,   IL12↓, 1,   IL1β↓, 2,   IL6↓, 1,   Inflam↓, 2,   IκB↑, 1,   MyD88↓, 1,   NF-kB↓, 3,   TLR2↓, 1,   TLR4↓, 1,   TNF-α↓, 1,   TRIF↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Clinical Biomarkers ⓘ

CRP↓, 2,   IL6↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 2,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 2,   RenoP↑, 1,   Weight∅, 1,  

Infection & Microbiome ⓘ

IRF3↓, 1,  
Total Targets: 62

Scientific Paper Hit Count for: TGF-β, transforming growth factor-beta
6 Thymoquinone
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#:304  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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