Thymoquinone / IL13 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)

IL13, Interleukin-13: Click to Expand ⟱

Source:

Type:

IL-13 - Interleukin-13

Type: Type-2 cytokine / immune signaling protein

Function: IL-13 is a type-2 immune cytokine produced by cells including group 2 innate lymphoid cells (ILC2), Th2 lymphocytes, mast cells, and eosinophils. IL-13 signals primarily through a receptor complex containing IL-13Rα1 and IL-4Rα, activating JAK/STAT6 and related pathways. It regulates alternative macrophage activation, mucus production, fibrosis, tissue remodeling, allergic inflammation, and type-2 immune responses.

Cancer: ↑ Frequently increased or functionally activated in tumor-associated type-2 immune responses. IL-13 can promote immunosuppressive macrophage polarization, stromal remodeling, fibrosis, tumor-cell survival, migration, invasion, and metastasis through IL-13 receptor and STAT6 signaling. Its effects remain tumor- and immune-context dependent.

Alzheimer's Disease: ↕ Context-dependent. IL-13 can modulate microglial and macrophage activation toward alternative immune phenotypes and may reduce selected pro-inflammatory responses, but its effects on amyloid pathology, neuroinflammation, and neuronal function vary by model and disease stage.

Scientific Papers found: Click to Expand⟱

7939-

TQ,

Effects of Nigella sativa and its constituents on inflammatory markers in ovalbumin-induced asthma model: a preclinical systematic review and meta-analysis

Review,

Asthma,

*IL4↓, *IL5↓, *IL13↓, *IL17↓, *IgE↓, *IFN-γ∅, *antiOx↑, *Inflam↓,

7940-

TQ,

Anti-inflammatory effect of thymoquinone in a mouse model of allergic lung inflammation

in-vivo,

Asthma,

mouse

*Eos↓, *Th2↓, *IgE↓, *IgG1↓, *Inflam↓, *AirwayM↓, *IL4↓, *IL5↓, *IL13↓, *IFN-γ↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:

Total Targets: 0

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AirwayM↓, 1, Eos↓, 1, IgE↓, 2, IgG1↓, 1, IL13↓, 2,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

IFN-γ↑, 1, IFN-γ∅, 1, IL17↓, 1, IL4↓, 2, IL5↓, 2, Inflam↓, 2, Th2↓, 1,
Total Targets: 13

Scientific Paper Hit Count for: IL13, Interleukin-13

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