Cinnamon / Glycolysis 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).

Glycolysis, Glycolysis: Click to Expand ⟱

Source:

Type:

Glycolysis is a metabolic pathway that converts glucose into pyruvate, producing a small amount of ATP (energy) in the process. It is a fundamental process for cellular energy production and occurs in the cytoplasm of cells. In normal cells, glycolysis is tightly regulated and is followed by aerobic respiration in the presence of oxygen, which allows for the efficient production of ATP.
In cancer cells, however, glycolysis is often upregulated, even in the presence of oxygen. This phenomenon is known as the Warburg Mutations in oncogenes (like MYC) and tumor suppressor genes (like TP53) can alter metabolic pathways, promoting glycolysis and other anabolic processes that support cell growth.effect.
Acidosis: The increased production of lactate from glycolysis can lead to an acidic microenvironment, which may promote tumor invasion and suppress immune responses.

Glycolysis is a hallmark of malignancy transformation in solid tumor, and LDH is the key enzyme involved in glycolysis.

Pathways:
-GLUTs, HK2, PFK, PK, PKM2, LDH, LDHA, PI3K/AKT/mTOR, AMPK, HIF-1a, c-MYC, p53, SIRT6, HSP90α, GAPDH, HBT, PPP, Lactate Metabolism, ALDO

Natural products targeting glycolytic signaling pathways https://pmc.ncbi.nlm.nih.gov/articles/PMC9631946/
Alkaloids:
-Berberine, Worenine, Sinomenine, NK007, Tetrandrine, N-methylhermeanthidine chloride, Dauricine, Oxymatrine, Matrine, Cryptolepine

Flavonoids: -Oroxyline A, Apigenin, Kaempferol, Quercetin, Wogonin, Baicalein, Chrysin, Genistein, Cardamonin, Phloretin, Morusin, Bavachinin, 4-O-methylalpinumisofavone, Glabridin, Icaritin, LicA, Naringin, IVT, Proanthocyanidin B2, Scutellarin, Hesperidin, Silibinin, Catechin, EGCG, EGC, Xanthohumol.

Non-flavonoid phenolic compounds:
Curcumin, Resveratrol, Gossypol, Tannic acid.

Terpenoids:
-Cantharidin, Dihydroartemisinin, Oleanolic acid, Jolkinolide B, Cynaropicrin, Ursolic Acid, Triptolie, Oridonin, Micheliolide, Betulinic Acid, Beta-escin, Limonin, Bruceine D, Prosapogenin A (PSA), Oleuropein, Dioscin.

Quinones:
-Thymoquinone, Lapachoi, Tan IIA, Emodine, Rhein, Shikonin, Hypericin

Others:
-Perillyl alcohol, HCA, Melatonin, Sulforaphane, Vitamin D3, Mycoepoxydiene, Methyl jasmonate, CK, Phsyciosporin, Gliotoxin, Graviola, Ginsenoside, Beta-Carotene.

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: Glycolysis, Glycolysis

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