Thymoquinone / IFN-γ 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)


IFN-γ, Interferon-γ: Click to Expand ⟱
Source:
Type:
Plays a key role in activation of cellular immunity and subsequently, stimulation of antitumor immune-response. Based on its cytostatic, pro-apoptotic and antiproliferative functions, IFN-γ is considered potentially useful for adjuvant immunotherapy for different types of cancer.
Moreover, it IFN-γ may inhibit angiogenesis in tumor tissue, induce regulatory T-cell apoptosis, and/or stimulate the activity of M1 proinflammatory macrophages to overcome tumor progression.
However, the current understanding of the roles of IFN-γ in the tumor microenvironment (TME) may be misleading in terms of its clinical application.

IFN-γ is often expressed in the tumor microenvironment, particularly in response to immune cell infiltration. Its expression can be influenced by the presence of tumor-infiltrating lymphocytes (TILs) and other immune cells.
High levels of IFN-γ are typically associated with a Th1 immune response, which is generally considered beneficial for anti-tumor immunity.

Tumor Suppression:
In many cases, IFN-γ has tumor-suppressive effects, as it can inhibit tumor cell proliferation and induce apoptosis in certain cancer types.


Scientific Papers found: Click to Expand⟱
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↓,
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↓,

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:


Redox & Oxidative Stress

ROS↑, 1,  

Cell Death

Apoptosis↑, 1,  

DNA Damage & Repair

DNAdam↑, 1,  

Cell Cycle & Senescence

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

EMT↓, 1,  

Migration

TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,  

Immune & Inflammatory Signaling

NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance

eff↑, 1,  
Total Targets: 11

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 2,   Catalase↑, 1,   GSH↑, 1,   GSTs↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MPO↓, 1,   NRF2↑, 1,   ROS↓, 2,   SOD↑, 1,   TAC↑, 1,   Thiols↑, 1,  

Cell Death

iNOS↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 2,   CXCc↓, 1,   IFN-γ↓, 2,   IL12↓, 1,   IL1β↓, 2,   IL6↓, 2,   Inflam↓, 2,   MCP1↓, 1,   MyD88↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TLR2↓, 1,   TLR4↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission

p‑tau↓, 1,  

Protein Aggregation

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 1,   BioAv↑, 1,   eff↑, 1,  

Clinical Biomarkers

IL6↓, 2,  

Functional Outcomes

cardioP↑, 2,   neuroP↑, 1,   RenoP↑, 1,  

Infection & Microbiome

IRF3↓, 1,  
Total Targets: 38

Scientific Paper Hit Count for: IFN-γ, Interferon-γ
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#:442  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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