Thymoquinone / Ki-67 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)


Ki-67, Ki-67 protein: Click to Expand ⟱
Source:
Type: proliferation marker
A high Ki-67 proliferation index means many cells are dividing quickly and that the cancer is likely to grow and spread.
Markers of proliferation index (Ki-67)

• Ki-67 serves primarily as a proliferation marker: higher levels are generally indicative of aggressive disease and poorer outcomes across many cancer types.
• While Ki-67 itself is not considered a driver of tumorigenesis, its expression mirrors the high proliferative activity associated with protumoral behavior.
• It is widely used in clinical practice to aid in tumor grading, prognostication, and treatment planning.
Scientific Papers found: Click to Expand⟱
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↓,
3573- TQ,    Chronic diseases, inflammation, and spices: how are they linked?
- Review, Var, NA
NF-kB↓, XIAP↓, PI3K↓, Akt↓, STAT3↓, JAK2↓, cSrc↓, PCNA↓, MMP2↓, ERK↓, Ki-67↓, Bcl-2↓, VEGF↓, p65↓, COX2↓, MMP9↓,
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↓,
1931- TQ,  doxoR,    Thymoquinone enhances the anticancer activity of doxorubicin against adult T-cell leukemia in vitro and in vivo through ROS-dependent mechanisms
- in-vivo, AML, NA
eff↑, tumCV↓, TumCCA↑, ROS↑, MMP↓, eff↑, TumVol↓, eff↑, Ki-67↓,
2121- TQ,    Thymoquinone Inhibits Tumor Growth and Induces Apoptosis in a Breast Cancer Xenograft Mouse Model: The Role of p38 MAPK and ROS
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
p‑p38↑, ROS↑, TumCP↓, eff↑, XIAP↓, survivin↓, Bcl-xL↓, Bcl-2↓, Ki-67↓, *Catalase↑, *SOD↑, *GSH↑, hepatoP↑, p‑MAPK↑, JNK↓, eff↓,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 4,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   XIAP↓, 3,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   PKM2↓, 1,   PPARγ↓, 1,   SIRT1↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 3,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 2,   Casp↑, 1,   Casp3↑, 2,   Casp7↑, 1,   Casp9↑, 2,   Cyt‑c↑, 1,   JNK↓, 1,   JNK↑, 1,   MAPK↑, 1,   p‑MAPK↑, 1,   p38↑, 1,   p‑p38↑, 1,   survivin↓, 3,  

Kinase & Signal Transduction ⓘ

cSrc↓, 2,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   H4↑, 1,   tumCV↓, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   P53↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   EMT↓, 1,   ERK↓, 1,   HDAC↓, 2,   HDAC1↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   Jun↓, 1,   mTOR↓, 2,   NOTCH↓, 1,   PI3K↓, 3,   PTEN↑, 2,   STAT3↓, 1,   p‑STAT3↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   FAK↓, 1,   Ki-67↓, 5,   MMP2↓, 1,   MMP9↓, 3,   MUC4↓, 1,   N-cadherin↓, 1,   TGF-β↓, 1,   TGF-β↑, 1,   TumCI↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   Twist↓, 1,   Vim↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 2,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   CXCR4↓, 1,   Inflam↓, 1,   JAK2↓, 2,   MCP1↓, 1,   NF-kB↓, 3,   p65↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   ChemoSen↑, 2,   Dose↝, 1,   eff↓, 1,   eff↑, 7,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

EZH2↓, 1,   Ki-67↓, 5,  

Functional Outcomes ⓘ

hepatoP↑, 2,   TumVol↓, 1,  
Total Targets: 85

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 2,   GPx↑, 1,   GSH↑, 2,   MDA↓, 1,   SOD↑, 2,  

Core Metabolism/Glycolysis ⓘ

NAD↑, 1,   SIRT1↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

CRP↓, 1,   IL6↓, 1,  
Total Targets: 17

Scientific Paper Hit Count for: Ki-67, Ki-67 protein
5 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#:425  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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