Thymoquinone / hTERT/TERT 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)


hTERT/TERT, human telomerase reverse transcriptase: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
A key component of the enzyme telomerase, which is responsible for maintaining the length of telomeres at the ends of chromosomes.
In most somatic cells, telomerase activity is low or absent, leading to progressive telomere shortening with each cell division, which eventually triggers cellular senescence or apoptosis. many cancer cells exhibit reactivation of telomerase, primarily through the upregulation of hTERT. This reactivation allows cancer cells to maintain their telomere length, enabling them to divide indefinitely and contributing to the immortality characteristic of cancer cells. The expression of hTERT is often associated with various types of cancer, including melanoma, breast cancer, and lung cancer.
| Cancer context | TERT biomarker                | Clinical use                             |
| -------------- | ----------------------------- | ---------------------------------------- |
| Glioma         | Promoter mutation             | **WHO classification, prognosis**        |
| Thyroid cancer | Promoter mutation             | **Aggressiveness, recurrence risk**      |
| Melanoma       | Promoter mutation             | Risk stratification                      |
| Bladder cancer | Promoter mutation (urine DNA) | **Noninvasive detection & surveillance** |
| HCC            | Promoter mutation             | Early event, prognosis                   |

Why TERT Is Valuable Despite Limited “Actionability”
-Telomere maintenance is mandatory for long-term tumor survival
-TERT activation is often an early, irreversible event
-Its presence signals a tumor that has escaped replicative limits
-That makes TERT one of the best markers of “point-of-no-return” biology.



Scientific Papers found: Click to Expand⟱
2095- TQ,    Review on the Potential Therapeutic Roles of Nigella sativa in the Treatment of Patients with Cancer: Involvement of Apoptosis
- Review, Var, NA
TumCCA↑, Apoptosis↑, ROS↑, Cyt‑c↑, Bax:Bcl2↑, Casp3↑, Casp9↑, cl‑PARP↑, P53↑, P21↑, cMyc↓, hTERT/TERT↓, cycD1/CCND1↓, CDK4↓, NF-kB↓, IAP1↓, IAP2↓, XIAP↓, Bcl-xL↓, survivin↓, COX2↓, MMP9↓, VEGF↓, 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↑,

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,  

Mitochondria & Bioenergetics

XIAP↓, 1,  

Core Metabolism/Glycolysis

cMyc↓, 2,  

Cell Death

Apoptosis↓, 1,   Apoptosis↑, 1,   Bax:Bcl2↑, 2,   Bcl-xL↓, 1,   Casp3↑, 2,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 2,   hTERT/TERT↓, 2,   IAP1↓, 1,   IAP2↓, 1,   survivin↓, 1,  

DNA Damage & Repair

P53↑, 2,   cl‑PARP↑, 2,  

Cell Cycle & Senescence

CDK4↓, 2,   cycD1/CCND1↓, 2,   P21↑, 2,   TumCCA↑, 1,  

Migration

MMP9↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature

VEGF↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance

eff↑, 1,   selectivity↑, 1,  

Clinical Biomarkers

hTERT/TERT↓, 2,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: hTERT/TERT, human telomerase reverse transcriptase
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#:150  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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