1,8-Cineole / TumCI Cancer Research Results

1,8-Cin, 1,8-Cineole: Click to Expand ⟱
Features:

1,8-Cineole — 1,8-cineole, also called eucalyptol, is a volatile bicyclic monoterpene ether and major active constituent of eucalyptus oil and several other aromatic plant oils (other plants such as oregano (Origanum spec.), thyme (Thymus spec.), guava (Psidium pohlianum) or sage (Salvia spec.)). Eucalyptus oil used for medicinal applications should contain at least 70% of 1,8-Cineol. It is best classified as a small-molecule phytochemical / essential-oil monoterpenoid rather than as a botanical extract. Its main established human-use identity is respiratory anti-inflammatory / mucolytic support, while its oncology relevance is preclinical and concentration-limited.

Primary mechanisms (ranked):

  1. Apoptosis induction through ↓ Akt / ↓ survivin with ↑ p38 MAPK, ↑ cleaved caspase-3, and ↑ cleaved PARP in colorectal cancer models.
  2. Suppression of PI3K / Akt / mTOR signaling linked to reduced migration and invasion in skin cancer models.
  3. Anti-proliferative and cell-cycle stress effects, including reduced BrdU incorporation and tumor-growth suppression in xenograft models.
  4. Oxidative-stress-linked apoptosis or senescence in selected models; this appears model-dependent and may require high concentrations.
  5. Anti-inflammatory cytokine suppression, including ↓ TNF-α and ↓ IL-1β, which is better established in inflammatory/airway contexts than as a direct cancer mechanism.
  6. Membrane penetration / formulation effects, relevant to delivery and topical/transmucosal exposure but not a cancer-selective mechanism.

Bioavailability / PK relevance: 1,8-cineole is orally and inhalationally absorbed and undergoes rapid systemic distribution, with CYP3A-mediated oxidation as an important metabolic route. Enteric-coated oral preparations can deliver measurable tissue exposure in airway/nasal tissues, but oncology-relevant systemic concentrations are not established.

In-vitro vs systemic exposure relevance: Many anticancer studies use millimolar-range in-vitro concentrations or concentrated essential-oil fractions, which likely exceed routine achievable systemic exposure from conventional oral or inhaled use. Direct cancer-cell effects should therefore be marked as exposure-constrained unless a delivery formulation is specified.

Clinical evidence status: Preclinical oncology only. There is cell-line and animal/xenograft evidence for anticancer activity, but no established cancer-directed clinical efficacy. Human clinical deployment is mainly respiratory/supportive use of eucalyptus oil or purified 1,8-cineole preparations, not antineoplastic therapy.

1,8-Cineole Cancer Mechanism Summary

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Akt / survivin / p38 apoptosis axis ↓ Akt; ↓ survivin; ↑ p38; ↑ cleaved PARP; ↑ caspase-3 Limited direct selectivity data G Apoptosis and tumor-growth suppression Core anticancer mechanism in colorectal cancer models; likely high-concentration dependent.
2 PI3K / Akt / mTOR invasion axis ↓ PI3K; ↓ Akt; ↓ mTOR; ↓ migration; ↓ invasion Not well established G Anti-invasive and anti-metastatic signaling Mechanistically central in skin cancer models; therapeutic translation remains preclinical.
3 Cell proliferation and cell-cycle stress ↓ proliferation; ↓ BrdU incorporation; ↑ growth arrest (model-dependent) Unclear G Cytostatic pressure and reduced tumor expansion Observed across multiple cancer models, but dose ranges often exceed routine clinical exposure.
4 ROS-linked apoptosis or senescence ↑ ROS (model-dependent); ↑ oxidative stress-linked death or senescence May show anti-inflammatory or antioxidant-context effects G Context-dependent oxidative stress leverage Evidence is mixed by model and preparation; stronger when using 1,8-cineole-rich extracts or high concentrations.
5 Inflammatory cytokine signaling Potential ↓ NF-κB-linked inflammatory support (context-dependent) ↓ TNF-α; ↓ IL-1β; ↓ airway inflammatory signaling R/G Anti-inflammatory modulation Better supported for airway/inflammatory disease than for direct cancer-cell killing.
6 Membrane penetration and formulation effects May alter uptake of co-administered compounds (context-dependent) Potential irritation or barrier disruption at high topical exposure R/G Delivery modifier Important for essential-oil and topical/transmucosal contexts; not inherently tumor-selective.
7 CYP3A metabolism and drug-interaction constraint ↔ direct anticancer effect CYP3A-mediated oxidation; systemic clearance R/G PK limitation Potential relevance for co-administered drugs, especially where CYP3A substrates or inhibitors are involved.
8 Clinical Translation Constraint High in-vitro concentrations may not map to systemic dosing GI irritation, CNS toxicity risk in overdose, pediatric laryngospasm/seizure precautions G Translation barrier Oncology status preclinical; established human use is respiratory/supportive rather than antineoplastic.

TSF legend: P: 0–30 min; R: 30 min–3 hr; G: >3 hr
TumCI, Tumor Cell invasion: Click to Expand ⟱
Source:
Type:
Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms:

1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion.

2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue.

3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment.

4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream.

5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body.

6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection.

7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs.

8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis.
Scientific Papers found: Click to Expand⟱
6465- 1,8-Cin,    Eucalyptol targets PI3K/Akt/mTOR pathway to inhibit skin cancer metastasis
- vitro+vivo, Melanoma, NA
TumMeta↓, TumCMig↓, TumCI↓, Vim↓, Snail↓, Slug↓, Twist↓, E-cadherin↓, EMT↓, MMP2↓, MMP9↓, PI3K↓, Akt↓, mTOR↓,

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,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   mTOR↓, 1,   PI3K↓, 1,  

Migration ⓘ

E-cadherin↓, 1,   MMP2↓, 1,   MMP9↓, 1,   Slug↓, 1,   Snail↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumMeta↓, 1,   Twist↓, 1,   Vim↓, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
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#:409  Target#:324  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

Home Page