Cinnamon / TumCI Cancer Research Results

Cin, Cinnamon: Click to Expand ⟱

Features:

Cinnamon is a spice from inner bark from several tree species.
Cinnamon refers primarily to bark extracts from Cinnamomum verum (Ceylon cinnamon) and Cinnamomum cassia. Bioactive constituents include cinnamaldehyde, cinnamic acid derivatives, procyanidins, and polyphenols. In cancer models, cinnamon extracts and cinnamaldehyde are most frequently reported to exert anti-proliferative, pro-apoptotic, anti-inflammatory, and anti-angiogenic effects. Mechanistic themes include suppression of NF-κB and PI3K/AKT signaling, modulation of MAPK pathways, induction of mitochondrial apoptosis, and context-dependent ROS elevation in tumor cells. Some studies report inhibition of HIF-1α and glycolytic signaling, though cinnamon is not a direct enzymatic Warburg inhibitor. Effects vary substantially depending on species (Ceylon vs Cassia), preparation (aqueous vs ethanol extract), and dose. Human oncology data remain limited and largely preclinical.

Biological activity, cinnamaldehyde from Ceylon cinnamon:
Antimicrobial activity: 10-50 μM
Antioxidant activity: 10-100 μM
Anti-inflammatory activity: 20-50 μM
Anticancer activity: 50-100 μM
Cardiovascular health: 20-50 μM

5 g of Ceylon cinnamon might contain roughly between 30 mg and 150 mg of cinnamaldehyde, with an approximate mid-range estimate of about 70 mg.
Assuming a moderate supplemental intake 50–200 mg of cinnamaldehyde, peak plasma levels might be anticipated in the vicinity of 1–10 μM.

Cancer Pathway Table: Cinnamon

Rank	Pathway / Axis	Cancer / Tumor Context	Normal Tissue Context	TSF	Primary Effect	Notes / Interpretation
1	NF-κB inflammatory / survival signaling	NF-κB ↓; COX-2 ↓; cytokines ↓ (reported)	Inflammatory tone ↓	R, G	Anti-inflammatory / anti-survival	One of the more consistently reported mechanisms across tumor models.
2	PI3K → AKT → mTOR axis	PI3K/AKT ↓; proliferation ↓ (model-dependent)	↔	R, G	Growth signaling suppression	Frequently observed downstream of cinnamaldehyde exposure.
3	Intrinsic apoptosis (mitochondrial pathway)	Bax ↑; Bcl-2 ↓; caspases ↑ (reported)	Minimal activation at lower exposure	G	Apoptotic induction	Apoptosis induction often associated with mitochondrial depolarization.
4	ROS modulation (dose-dependent)	ROS ↑ (tumor contexts); apoptosis ↑	Antioxidant activity at low exposure	P, R	Redox modulation	Cinnamaldehyde may increase ROS in cancer cells while acting antioxidant at lower doses.
5	MAPK pathways (ERK / JNK / p38)	Stress-MAPK modulation (context-dependent)	↔	P, R, G	Signal reprogramming	JNK/p38 activation reported in apoptosis models; ERK modulation varies.
6	HIF-1α / glycolysis signaling	HIF-1α ↓; glycolytic gene expression ↓ (reported)	↔	R, G	Indirect Warburg modulation	Not a direct enzyme inhibitor; metabolic effects appear secondary to survival pathway suppression.
7	Angiogenesis (VEGF signaling)	VEGF ↓; angiogenesis ↓ (reported)	↔	G	Anti-angiogenic	Observed in some in vitro and animal models.
8	Cell-cycle regulation (G1/G2-M arrest)	Cell-cycle arrest ↑ (reported)	↔	G	Cytostasis	Associated with reduced Cyclin/CDK expression.
9	Metastasis / EMT modulation	MMPs ↓; migration ↓ (reported)	↔	G	Anti-invasive phenotype	Likely downstream of NF-κB and PI3K modulation.
10	Safety / composition constraint (coumarin content)	High cassia intake may pose hepatotoxicity risk	Generally safe in culinary amounts	—	Translation constraint	Cassia cinnamon contains higher coumarin; Ceylon cinnamon preferred for higher intake.

TSF: P = 0–30 min (redox and early signaling effects), R = 30 min–3 hr (acute pathway modulation), G = >3 hr (apoptosis, angiogenesis, phenotype changes).

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⟱

1274-

Cin,

Cinnamon bark extract suppresses metastatic dissemination of cancer cells through inhibition of glycolytic metabolism

vitro+vivo,

BC,

MDA-MB-231

TumCI↓, G6PD↓, HK2↓, Glycolysis↓,

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:

Core Metabolism/Glycolysis ⓘ

G6PD↓, 1, Glycolysis↓, 1, HK2↓, 1,

Migration ⓘ

TumCI↓, 1,
Total Targets: 4

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