Thymoquinone / selectivity 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)


selectivity, selectivity: Click to Expand ⟱
Source:
Type:
The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues.

Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance

Factors that affect selectivity:
1. Ability of Cancer cells to preferentially absorb a product/drug
-EPR-enhanced permeability and retention of cancer cells
-nanoparticle formations/carriers may target cancer cells over normal cells
-Liposomal formations. Also negatively/positively charged affects absorbtion

2. Product/drug effect may be different for normal vs cancer cells
- hypoxia
- transition metal content levels (iron/copper) change probability of fenton reaction.
- pH levels
- antiOxidant levels and defense levels

3. Bio-availability
Scientific Papers found: Click to Expand⟱
3421- TQ,    Insights into the molecular interactions of thymoquinone with histone deacetylase: evaluation of the therapeutic intervention potential against breast cancer
- Analysis, Nor, NA - in-vivo, Nor, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, HaCaT
HDAC↓, P21↑, Maspin↑, BAX↑, B2M↓, TumCCA↑, selectivity↑, *toxicity↓, TumCMig↓, TumCP↓,
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↓,
3424- TQ,    Thymoquinone Is a Multitarget Single Epidrug That Inhibits the UHRF1 Protein Complex
- Review, Var, NA
DNMT1↓, HDAC1↓, TumCCA↑, ROS↑, Apoptosis↑, angioG↓, TumMeta↓, selectivity↑, BioAv↓, BioAv↓, HDAC1↓, HDAC4↓, UHRF1↓, selectivity↑, G9a↓,
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↑,
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↝,
2093- TQ,    Regulation of NF-κB Expression by Thymoquinone; A Role in Regulating Pro-Inflammatory Cytokines and Programmed Cell Death in Hepatic Cancer Cells
- in-vitro, Liver, HepG2 - in-vitro, Nor, NA
TumCD↑, selectivity↑, Casp3↑, DLC1↑, NF-kB↑, LDH↑, *toxicity↓,
2096- TQ,    Effect of total hydroalcholic extract of Nigella sativa and its n-hexane and ethyl acetate fractions on ACHN and GP-293 cell lines
- in-vitro, Nor, GP-293 - in-vitro, Kidney, ACHN
selectivity↑, eff↝,
2097- TQ,    Crude extract of Nigella sativa inhibits proliferation and induces apoptosis in human cervical carcinoma HeLa cells
- in-vitro, Cerv, HeLa
Cyt‑c↑, Bax:Bcl2↑, Casp3↑, Casp9↑, Casp8↑, cl‑PARP↑, cMyc↓, hTERT/TERT↓, cycD1/CCND1↓, CDK4↓, P53↑, P21↑, TumCP↓, Apoptosis↓, selectivity↑,
1935- TQ,    Potential anticancer properties and mechanisms of thymoquinone in osteosarcoma and bone metastasis
- Review, OS, NA
Apoptosis↑, TumCCA↑, angioG↓, TumMeta↓, ROS↑, P53↑, Twist↓, E-cadherin↑, N-cadherin↓, NF-kB↓, IL8↓, XIAP↓, Bcl-2↓, STAT3↓, MAPK↓, PI3K↓, Akt↓, ERK↓, MMP2↓, MMP9↓, *ROS↓, HO-1↑, selectivity↑, TumCG↓,
1936- TQ,    Thymoquinone induces apoptosis and increase ROS in ovarian cancer cell line
- in-vitro, Ovarian, CaOV3 - in-vitro, Nor, WRL68
selectivity↑, TumCP↓, MMP↓, Bcl-2↓, BAX↑, ROS↑,
2124- TQ,    Thymoquinone: an emerging natural drug with a wide range of medical applications
- Review, Var, NA
hepatoP↑, Bax:Bcl2↑, cycD1/CCND1↓, P21↑, TRAIL↑, P53↑, TumCCA↑, hepatoP↑, *ALAT↓, *AST↓, *MDA↓, *GSSG↓, *COX2↓, *lipid-P↓, PPARγ↑, p38↑, ROS↑, ChemoSen↑, selectivity↑, selectivity↑, *MDA↓, *SOD↑,
2106- TQ,    Cancer: Thymoquinone antioxidant/pro-oxidant effect as potential anticancer remedy
- Review, Var, NA
Apoptosis↑, TumCCA↑, ROS↑, *Catalase↑, *SOD↑, *GR↑, *GSTA1↓, *GPx↑, *H2O2↓, *ROS↓, *lipid-P↓, *HO-1↑, p‑Akt↓, AMPKα↑, NK cell↑, selectivity↑, Dose↝, eff↑, GSH↓, eff↓, P53↑, p‑STAT3↓, PI3K↑, MAPK↑, GSK‐3β↑, ChemoSen↑, RadioS↑, BioAv↓, NRF2↑,
2110- TQ,    Nigella sativa seed oil suppresses cell proliferation and induces ROS dependent mitochondrial apoptosis through p53 pathway in hepatocellular carcinoma cells
- in-vitro, HCC, HepG2 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, Nor, HEK293
P53↑, lipid-P↑, GSH↓, ROS↑, MMP↓, BAX↑, Casp3↑, Casp9↑, Bcl-2↓, tumCV↓, selectivity↑,

Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 2,   HO-1↑, 1,   lipid-P↑, 1,   NRF2↑, 1,   ROS↑, 9,   ROS⇅, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 3,   LDH↑, 1,   PPARγ↓, 1,   PPARγ↑, 1,   SIRT1↓, 1,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 5,   BAX↑, 5,   Bax:Bcl2↑, 2,   Bcl-2↓, 5,   Bcl-2↑, 1,   Bcl-xL↓, 2,   Casp↑, 1,   Casp3↑, 5,   Casp7↑, 2,   Casp8↑, 1,   Casp9↑, 4,   Cyt‑c↑, 1,   hTERT/TERT↓, 1,   IAP1↓, 1,   IAP2↑, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p27↑, 1,   p38↑, 2,   survivin↓, 3,   TRAIL↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,   cSrc↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 2,   G9a↓, 1,   P53↑, 7,   cl‑PARP↑, 4,   UHRF1↓, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 5,   P21↑, 4,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 3,   ERK↓, 2,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   HDAC↓, 2,   HDAC1↓, 3,   HDAC2↓, 1,   HDAC3↓, 1,   HDAC4↓, 1,   miR-34a↑, 1,   mTOR↓, 3,   NOTCH↓, 1,   PI3K↓, 4,   PI3K↑, 1,   PTEN↑, 3,   STAT3↓, 2,   p‑STAT3↓, 2,   TumCG↓, 1,  

Migration ⓘ

DLC1↑, 1,   E-cadherin↓, 1,   E-cadherin↑, 2,   Ki-67↓, 1,   MMP2↓, 1,   MMP9↓, 2,   MMPs↓, 1,   MUC4↓, 1,   N-cadherin↓, 2,   Rac1↓, 1,   TumCMig↓, 1,   TumCP↓, 4,   TumMeta↓, 3,   Twist↓, 4,   Vim↓, 1,   Zeb1↓, 1,   α-tubulin↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

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

Immune & Inflammatory Signaling ⓘ

B2M↓, 1,   COX2↓, 2,   CXCR4↓, 1,   IL8↓, 1,   Inflam↓, 1,   IκB↓, 1,   JAK2↓, 1,   NF-kB↓, 3,   NF-kB↑, 1,   p‑NF-kB↑, 1,   NK cell↑, 1,   p‑p65↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 4,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 5,   Dose↝, 1,   eff↓, 1,   eff↑, 4,   eff↝, 1,   RadioS↑, 3,   selectivity↑, 15,  

Clinical Biomarkers ⓘ

AR↓, 1,   B2M↓, 1,   EZH2↓, 1,   hTERT/TERT↓, 1,   Ki-67↓, 1,   LDH↑, 1,   Maspin↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   chemoPv↑, 1,   hepatoP↑, 3,  
Total Targets: 128

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 3,   GPx↑, 3,   GSH↑, 1,   GSSG↓, 1,   GSTA1↓, 1,   GSTA1↑, 1,   H2O2↓, 1,   HO-1↑, 1,   lipid-P↓, 2,   MDA↓, 3,   ROS↓, 3,   SOD↑, 4,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   NAD↑, 1,   SIRT1↑, 1,  

Migration ⓘ

MMP13↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling ⓘ

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

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   CRP↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

chemoPv↑, 1,   hepatoP↑, 1,   toxicity↓, 2,  
Total Targets: 37

Scientific Paper Hit Count for: selectivity, selectivity
13 Thymoquinone
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#:1110  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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