Turmerones / PI3K Cancer Research Results

TUR, Turmerones: Click to Expand ⟱
Features:

Turmerones — Turmerones are lipophilic volatile sesquiterpenes from turmeric rhizome oil, mainly ar-turmerone, α-turmerone, and β-turmerone. They are distinct from curcuminoids and should not be treated as curcumin synonyms. Formal classification: plant-derived volatile oil constituents / sesquiterpene ketones. Standard abbreviations include ATM or ar-T for aromatic turmerone, and α-TUR / β-TUR for α- and β-turmerone. Separate database product from whole turmeric or curcumin, because turmerones have different PK, BBB penetration, P-gp modulation, and apoptosis mechanisms from curcumin.

Primary mechanisms (ranked):

  1. ROS-linked mitochondrial and death-receptor apoptosis, especially reported for ar-turmerone in hepatocellular carcinoma and leukemia models.
  2. Growth suppression and programmed cell death in selected cancer cell lines, with strongest support in preclinical leukemia and hepatocellular carcinoma studies.
  3. Migration and invasion suppression in glioma models through cathepsin B and P27-related signaling.
  4. Inflammation and stress-pathway modulation, including NF-κB, JNK, p38 MAPK, COX-2, iNOS, cytokines, and MMP-related axes, mostly context-dependent.
  5. Curcumin bioavailability and transporter modulation, including altered Caco-2 transport and mixed P-gp effects depending on the turmerone isomer.

Bioavailability / PK relevance: Turmerones are more lipophilic than curcumin and are relevant as turmeric-oil constituents and as curcumin bioavailability modifiers. Reported animal PK suggests measurable systemic exposure, moderate oral bioavailability for major turmeric-oil constituents, and meaningful brain distribution. Human therapeutic PK for isolated turmerones remains insufficient.

In-vitro vs systemic exposure relevance: Many anticancer experiments use tens of μg/mL concentrations, which may exceed typical achievable free systemic exposure after ordinary turmeric intake. Turmeric oil or enriched turmerone formulations may increase exposure, but cancer-cell IC50 values should be treated as preclinical screening concentrations rather than clinically validated dosing targets.

Clinical evidence status: Preclinical. There is no strong cancer clinical-trial evidence for isolated turmerones. Human turmeric oil safety data and curcumin/turmeric-formulation trials do not establish turmerone-specific oncology efficacy. Recommended database status: add as a separate mechanistic/preclinical product, linked to turmeric oil and curcumin as related entries.

Turmerones Cancer Mechanism Table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial ROS apoptosis ↑ ROS, ↓ mitochondrial membrane potential, ↑ Bax, ↑ PUMA, ↑ cytochrome c release, ↑ caspase-9, ↑ caspase-3 Likely lower selectivity margin not fully established R/G Apoptosis induction Core ar-turmerone mechanism in hepatocellular carcinoma models; high concentration only; model-dependent
2 Death receptor apoptosis ↑ Fas, ↑ DR4, ↑ caspase-8, ↑ caspase-3 Insufficient direct comparison R/G Extrinsic apoptosis support Appears coupled to ROS and MAPK stress signaling rather than a fully independent primary trigger
3 JNK and ERK stress signaling ↑ JNK, ↑ ERK, ↑ pro-apoptotic signaling Context-dependent R/G Amplifies apoptosis Stress-kinase activation appears downstream of ROS in hepatocellular carcinoma models
4 Programmed cell death in leukemia ↑ DNA fragmentation, ↑ apoptotic morphology, ↓ viability Some selectivity reported versus selected non-target cells, but evidence remains limited G Cytotoxic apoptosis Older but relevant evidence supports ar-turmerone and related turmeric-oil constituents as apoptosis inducers in leukemia models
5 Glioma cathepsin B and P27 axis ↓ cathepsin B, ↓ P27 cleavage, ↓ proliferation, ↓ mobility Not well defined G Reduced proliferation and migration Potential CNS-oncology relevance because ar-turmerone is brain-penetrant; still preclinical
6 NF-κB inflammatory axis ↔/↓ NF-κB depending on model and stimulus ↓ NF-κB activation in inflammatory microglial models R/G Anti-inflammatory and context-dependent anticancer support curcuminoids suppress NF-κB more consistently than turmerones in some comparative studies
7 COX-2 iNOS MMP inflammatory mediators ↓ COX-2, ↓ MMP-related signaling (context-dependent) ↓ iNOS, ↓ COX-2, ↓ MMP-9 in activated microglia G Reduced inflammatory mediator output More relevant to inflammation, tumor microenvironment, and AD than direct tumor killing
8 P-gp and curcumin transport ↔ P-gp activity depending on isomer; ↑ curcumin cellular transport in Caco-2 model ↔ drug-transporter interaction risk R Bioavailability and drug-interaction modulation α-turmerone and ar-turmerone have different transporter effects; this is a key reason to keep turmerones separate from curcumin
9 Chemosensitization Possible ↑ intracellular exposure of co-administered compounds through transporter effects Possible altered exposure to normal tissues R/G Unproven adjunct potential Mechanistically plausible but not clinically established for oncology; not a strong chemosensitizer
10 Clinical Translation Constraint Preclinical activity often requires high μg/mL concentrations Oral oil safety appears better supported than isolated high-dose oncology use G Limits clinical confidence Major constraints are exposure, formulation, isomer composition, lack of isolated-turmerone cancer trials, and potential transporter-mediated interactions

P:0–30 min R:30 min–3 hr G:>3 hr
PI3K, Phosphatidylinositide-3-Kinases: Click to Expand ⟱
Source: HalifaxProj(inhibit) CGL-CS
Type:
Phosphatidylinositol 3-kinase (PtdIns3K or PI3K) is a family of enzymes that play a crucial role in cell signaling pathways, particularly in the regulation of cell growth, survival, and metabolism. The PI3K pathway is one of the most frequently altered pathways in human cancer. Inhibition of the PI3K pathway has been explored as a therapeutic strategy for cancer treatment. Several PI3K inhibitors have been developed and are currently being tested in clinical trials. These inhibitors can target specific components of the pathway, such as PI3K, AKT, or mTOR.

Class I phosphoinositide 3-kinase (PI3K)
Class III PtdIns3K
In contrast to the class III PtdIns3K as a positive regulator of autophagy, class I PI3K-AKT signaling has an opposing effect on the initiation of autophagy.

PI3K inhibitors include:
-Idelalisib , Copanlisib, Alpelisib
-LY294002?
-Wortmannin: potent PI3K inhibitor, has some associated toxicity.
-Quercetin:
-Curcumin
-Resveratrol
-Epigallocatechin Gallate (EGCG)
Scientific Papers found: Click to Expand⟱
6452- TUR,    Turmeric Essential Oil Constituents as Potential Drug Candidates: A Comprehensive Overview of Their Individual Bioactivities
- Review, Nor, NA
Dose↝, Casp3↑, MMP9↓, COX2↓, NF-kB↓, PI3K↓, Akt↓, ERK↓, Inflam↓, TNF-α↓, IL6↓, IL17↓, IL22↓, IL23↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

Akt↓, 1,   Casp3↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   PI3K↓, 1,  

Migration ⓘ

MMP9↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL17↓, 1,   IL22↓, 1,   IL23↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PI3K, Phosphatidylinositide-3-Kinases
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#:408  Target#:252  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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