Thymoquinone / HDAC1 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)


HDAC1, Histone Deacetylase 1: Click to Expand ⟱
Source:
Type:
HDAC1 is an enzyme that removes acetyl groups from histone tails, resulting in chromatin condensation and transcriptional repression.
– By modulating the acetylation status of histones, HDAC1 plays a key role in regulating gene expression involved in cell cycle progression, differentiation, apoptosis, and DNA repair.
– Aberrant expression or activity of HDAC1 has been linked to several cancers.
– Overexpression of HDAC1 can lead to the repression of tumor suppressor genes, thereby promoting oncogenic programs and contributing to tumor progression.
– HDAC1 is often associated with a more aggressive tumor phenotype and, in some contexts, a poorer clinical prognosis.
Therapeutic Targeting:
– HDAC inhibitors (HDACis) have emerged as anticancer agents; they work by inhibiting HDAC activity to restore acetylation levels on histones and nonhistone proteins.
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↓,
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↓,
3423- TQ,    Epigenetic role of thymoquinone: impact on cellular mechanism and cancer therapeutics
- Review, Var, NA
AntiCan↑, Inflam↓, hepatoP↑, RenoP↑, BAX↑, Bak↑, Bcl-2↓, Bcl-xL↓, ROS↑, P53↑, PTEN↑, P21↑, p27↑, BRCA1↑, PI3K↓, Akt↓, MAPK↓, ERK↓, p‑ERK↓, MMPs↓, FAK↓, Twist↓, Zeb1↓, EMT↓, TumMeta↓, angioG↓, VEGF↓, HDAC↓, Maspin↑, SIRT1↑, DNMT1↓, DNMT3A↓, HDAC1↓, HDAC4↓,
3427- TQ,    Chemopreventive and Anticancer Effects of Thymoquinone: Cellular and Molecular Targets
ROS⇅, Fas↑, DR5↑, TRAIL↑, Casp3↑, Casp8↑, Casp9↑, P53↑, mTOR↓, Bcl-2↓, BID↓, CXCR4↓, JNK↑, p38↑, MAPK↑, LC3II↑, ATG7↑, Beclin-1↑, AMPK↑, PPARγ↑, eIF2α↓, P70S6K↓, VEGF↓, ERK↓, NF-kB↓, XIAP↓, survivin↓, p65↓, DLC1↑, FOXO↑, TET2↑, CYP1B1↑, UHRF1↓, DNMT1↓, HDAC1↓, IL2↑, IL1↓, IL6↓, IL10↓, IL12↓, TNF-α↓, iNOS↓, COX2↓, 5LO↓, AP-1↓, PI3K↓, Akt↓, cMET↓, VEGFR2↓, CXCL1↓, ITGA5↓, Wnt↓, β-catenin/ZEB1↓, GSK‐3β↓, Myc↓, cycD1/CCND1↓, N-cadherin↓, Snail↓, Slug↓, Vim↓, Twist↓, Zeb1↓, MMP2↓, MMP7↓, MMP9↓, JAK2↓, STAT3↓, NOTCH↓, cycA1/CCNA1↓, CDK2↓, CDK4↓, CDK6↓, CDC2↓, CDC25↓, Mcl-1↓, E2Fs↓, p16↑, p27↑, P21↑, ChemoSen↑,
3426- TQ,    Thymoquinone-Induced Reactivation of Tumor Suppressor Genes in Cancer Cells Involves Epigenetic Mechanisms
- in-vitro, BC, MDA-MB-468 - in-vitro, AML, JK
UHRF1↓, DNMT1↓, DNMT3A↓, DNMTs↓, HDAC1↓, HDAC4↓, HDAC↓, DLC1↑, PPARγ↑, FOXO↑, TET2↑, CYP1B1↑, G9a↓,
2104- TQ,    The Potential Role of Nigella sativa Seed Oil as Epigenetic Therapy of Cancer
- in-vitro, BC, MCF-7 - in-vitro, Cerv, HeLa
TumCP↓, Apoptosis↑, UHRF1↓, DNMT1↓, HDAC1↓, eff↝,
2105- TQ,    Thymoquinone Promotes Pancreatic Cancer Cell Death and Reduction of Tumor Size through Combined Inhibition of Histone Deacetylation and Induction of Histone Acetylation
- in-vitro, PC, AsPC-1 - in-vitro, PC, MIA PaCa-2 - in-vitro, PC, Hs766t - in-vivo, NA, NA
tumCV↓, TumCP↓, TumCCA↑, Apoptosis↑, P53↑, Bcl-2↓, P21↑, ac‑H4↑, HDAC↓, HDAC1↓, HDAC2↓, HDAC3↓, TumVol↓,

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 3,   ROS⇅, 1,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   CDC25↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   ATG7↑, 1,   cMyc↓, 1,   PPARγ↓, 1,   PPARγ↑, 2,   SIRT1↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 3,   Apoptosis↑, 4,   Bak↑, 1,   BAX↑, 2,   Bcl-2↓, 4,   Bcl-xL↓, 2,   BID↓, 1,   Casp↑, 1,   Casp3↑, 2,   Casp7↑, 1,   Casp8↑, 1,   Casp9↑, 2,   DR5↑, 1,   Fas↑, 1,   iNOS↓, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   Myc↓, 1,   p27↑, 2,   p38↑, 1,   survivin↓, 2,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

cSrc↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   ac‑H4↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

BRCA1↑, 1,   CYP1B1↑, 2,   DNMT1↓, 6,   DNMT3A↓, 2,   DNMTs↓, 1,   G9a↓, 2,   p16↑, 1,   P53↑, 4,   cl‑PARP↑, 1,   UHRF1↓, 4,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 2,   E2Fs↓, 1,   P21↑, 3,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 1,   EMT↓, 2,   ERK↓, 2,   p‑ERK↓, 1,   FOXO↑, 2,   GSK‐3β↓, 1,   HDAC↓, 4,   HDAC1↓, 8,   HDAC2↓, 2,   HDAC3↓, 2,   HDAC4↓, 3,   mTOR↓, 2,   NOTCH↓, 1,   P70S6K↓, 1,   PI3K↓, 3,   PTEN↑, 2,   STAT3↓, 1,   p‑STAT3↓, 1,   Wnt↓, 1,  

Migration ⓘ

5LO↓, 1,   AP-1↓, 1,   DLC1↑, 2,   E-cadherin↑, 1,   FAK↓, 1,   ITGA5↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP7↓, 1,   MMP9↓, 2,   MMPs↓, 1,   N-cadherin↓, 2,   Slug↓, 1,   Snail↓, 1,   TumCP↓, 2,   TumMeta↓, 2,   Twist↓, 3,   Vim↓, 2,   Zeb1↓, 3,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

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

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CXCL1↓, 1,   CXCR4↓, 2,   IL1↓, 1,   IL10↓, 1,   IL12↓, 1,   IL2↑, 1,   IL6↓, 1,   Inflam↓, 1,   JAK2↓, 2,   NF-kB↓, 2,   p65↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↝, 1,   ChemoSen↑, 2,   eff↑, 3,   eff↝, 1,   RadioS↑, 1,   selectivity↑, 3,   TET2↑, 2,  

Clinical Biomarkers ⓘ

BRCA1↑, 1,   EZH2↓, 1,   IL6↓, 1,   Ki-67↓, 1,   Maspin↑, 1,   Myc↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   hepatoP↑, 2,   RenoP↑, 1,   TumVol↓, 1,  
Total Targets: 134

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

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

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: HDAC1, Histone Deacetylase 1
7 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#:982  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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