Database Query Results : Thymoquinone, , FAK

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)


FAK, FAK signaling: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
FAK (Focal Adhesion Kinase) is a non-receptor tyrosine kinase that plays a crucial role in cellular processes such as adhesion, migration, proliferation, and survival. It is primarily localized at focal adhesions, where it interacts with integrins and other signaling molecules. FAK promotes cell proliferation by activating signaling pathways such as the PI3K/Akt and MAPK/ERK pathways. These pathways are often upregulated in cancer cells, leading to uncontrolled growth.
Scientific Papers found: Click to Expand⟱
3423- TQ,    Epigenetic role of thymoquinone: impact on cellular mechanism and cancer therapeutics
- Review, Var, NA
AntiCan↑, Thymoquinone is a natural product with anticancer activity.
Inflam↓, Thymoquinone has been shown to exert anti-inflammatory, antidiabetic, antihypertensive, antimicrobial, analgesic, immunomodulatory, spasmolytic, hepatoprotective, renal-protective, gastroprotective, bronchodilatory, antioxidant and antineoplastic eff
hepatoP↑,
RenoP↑,
BAX↑, Thymoquinone can upregulate proapoptotic genes and proteins, such as Bax/Bak, or downregulate antiapoptotic genes and proteins, such as Bcl-2, Bcl-xL, among others, as well as modulating the caspase pathway
Bak↑,
Bcl-2↓,
Bcl-xL↓,
ROS↑, through the generation of reactive oxygen species (ROS)
P53↑, overexpressed or activated by thymoquinone; for example, p53, PTEN, p21, p27 and breast cancer type 1 susceptibility protein (BRCA1), among others,
PTEN↑,
P21↑,
p27↑,
BRCA1↑,
PI3K↓, (PI3K)/Akt and mitogen-activated protein kinase (MAPK)/ERK, have been found to be inhibited by thymoquinone
Akt↓,
MAPK↓,
ERK↓,
p‑ERK↓, thymoquinone reduces ERK phosphorylation and matrix metalloproteinase (MMP) secretion by downregulating focal adhesion kinase (FAK)
MMPs↓,
FAK↓,
Twist↓, downregulates Twist1 and Zeb1 transcription factors, and thus inhibits epithelial to mesenchymal transition (EMT) and subsequently inhibits cancer metastasis
Zeb1↓,
EMT↓,
TumMeta↓,
angioG↓, thymoquinone can inhibit angiogenesis by interfering with essential steps of neovascularization, such as suppressing proangiogenic vascular endothelial growth factor (VEGF)
VEGF↓,
HDAC↓, HDACs are usually overexpressed in MCF-7 breast cancer cells, and thymoquinone can act as a HDAC inhibitor (HDACi) that potently induces apoptosis through inducing acetylation of histones and inhibiting deacetylation of histones.
Maspin↑, thymoquinone reactivates HDAC target genes (p21 and Maspin), inducing the upregulation of Bax
SIRT1↑, thymoquinone can upregulate SIRT1 expression in neonatal rat cardiomyocytes and consequently deacetylates p53; thus, it can act as an apoptosis inducer
DNMT1↓, Collectively, they suggested that thymoquinone induces methylation of DNA via binding with DNMT1 and suppressing its expression,
DNMT3A↓, thymoquinone decreases the expression of some important epigenetic proteins like DNMT1,3A,3B, G9A, HDAC1,4,9, KDM1B, KMT2A,B,C,D,E and UHRF1 in Jurkat cells,
HDAC1↓,
HDAC4↓,

3425- TQ,    Advances in research on the relationship between thymoquinone and pancreatic cancer
Apoptosis↑, TQ can inhibit cell proliferation, promote cancer cell apoptosis, inhibit cell invasion and metastasis, enhance chemotherapeutic sensitivity, inhibit angiogenesis, and exert anti-inflammatory effects.
TumCP↓,
TumCI↓,
TumMeta↓,
ChemoSen↑,
angioG↓,
Inflam↓,
NF-kB↓, These anticancer effects predominantly involve the nuclear factor (NF)-κB, phosphoinositide 3 kinase (PI3K)/Akt, Notch, transforming growth factor (TGF)-β, c-Jun N-terminal kinase (JNK)
PI3K↓,
Akt↓,
TGF-β↓,
Jun↓,
p38↑, and p38 mitogen-activated protein kinase (MAPK) signaling pathways as well as the regulation of the cell cycle, matrix metallopeptidase (MMP)-9 expression, and pyruvate kinase isozyme type M2 (PKM2) activity.
MAPK↑, activation of the JNK and p38 MAPK
MMP9↓,
PKM2↓, decrease in PKM2 activity
ROS↑, ROS-mediated activation
JNK↑, activation of the JNK and p38 MAPK
MUC4↓, downregulation of MUC4;
TGF-β↑, TQ led to the activation of the TGF-β pathway and subsequent downregulation of MUC4
Dose↝, Q acts as an antioxidant (free radical scavenger) at low concentrations and as a pro-oxidant at high concentrations.
FAK↓, TQ can inhibit several key molecules such as FAK, Akt, NF-κB, and MMP-9 and that these molecules interact in a cascade to affect the metastasis of pancreatic cancer
NOTCH↓, TQ involved in increasing chemosensitivity consist of blocking the Notch1/PTEN, PI3K/Akt/mTOR, and NF-κB signaling pathways, reducing PKM2 expression, and inhibiting the Warburg effect.
PTEN↑, it also restored the PTEN protein that had been inhibited by GEM
mTOR↓,
Warburg↓, reducing PKM2 expression, and inhibiting the Warburg effect.
XIAP↓,
COX2↓,
Casp9↑,
Ki-67↓,
CD34↓,
VEGF↓,
MCP1↓,
survivin↓,
Cyt‑c↑,
Casp3↑,
H4↑,
HDAC↓,


* 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↑, 2,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

PKM2↓, 1,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   p27↑, 1,   p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

H4↑, 1,  

DNA Damage & Repair ⓘ

BRCA1↑, 1,   DNMT1↓, 1,   DNMT3A↓, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   EMT↓, 1,   ERK↓, 1,   p‑ERK↓, 1,   HDAC↓, 2,   HDAC1↓, 1,   HDAC4↓, 1,   Jun↓, 1,   mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 2,   PTEN↑, 2,  

Migration ⓘ

FAK↓, 2,   Ki-67↓, 1,   MMP9↓, 1,   MMPs↓, 1,   MUC4↓, 1,   TGF-β↓, 1,   TGF-β↑, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 2,   Twist↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 2,   MCP1↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↝, 1,  

Clinical Biomarkers ⓘ

BRCA1↑, 1,   Ki-67↓, 1,   Maspin↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   hepatoP↑, 1,   RenoP↑, 1,  
Total Targets: 64

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: FAK, FAK signaling
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#:110  State#:%  Dir#:%
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