Cinnamon / mTOR 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.

-Cinnamaldehyde (CA), an active compound derived from the natural plant cinnamon. CA is an aromatic aldehyde compound, constituting approximately 65% of cinnamon extract
- See also HCA, a derivative of CA

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.

Primary mechanisms (ranked):

  1. Suppression of inflammatory and survival signaling, especially NF-κB, AP-1, COX-2, PI3K/AKT, and related anti-apoptotic programs.
  2. Induction of mitochondrial apoptosis and cell-cycle arrest in cancer models.
  3. Anti-metastatic and anti-invasive effects linked to glycolysis/HK2 suppression, migration inhibition, and EMT-related signaling changes.
  4. Anti-angiogenic activity through VEGF/VEGFR2/HIF-1α and downstream MAPK signaling modulation.
  5. Redox modulation, with antioxidant/NRF2 activation in normal-cell stress contexts but ROS elevation and apoptosis in some tumor models.

Bioavailability / PK relevance: Cinnamon is compositionally variable; cinnamaldehyde is lipophilic, rapidly absorbed and metabolized, and systemic exposure after oral intake is likely much lower than many in-vitro anticancer concentrations. Extract formulation, species, dose, food matrix, and first-pass metabolism materially affect exposure.

In-vitro vs systemic exposure relevance: Many anticancer studies use extract concentrations or cinnamaldehyde levels that may exceed achievable free systemic exposure after ordinary oral intake. Local gastrointestinal exposure may be more plausible than systemic tumor exposure.

Clinical evidence status: Preclinical for oncology. Cinnamon has human RCT/meta-analysis literature mainly in metabolic/inflammatory endpoints, but no established clinical anticancer indication. Translational constraints include variable extract chemistry, cassia coumarin hepatotoxicity risk, CYP/herb-drug interaction potential, and uncertain tumor-achievable exposure.

Cinnamon Cancer Mechanism Table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 NF-κB AP-1 inflammatory survival signaling NF-κB ↓; AP-1 ↓; COX-2 ↓; Bcl-2 family survival tone ↓ Inflammatory tone ↓ R, G Anti-inflammatory and anti-survival signaling Core mechanism for cinnamon extract and cinnamaldehyde; model-dependent but repeatedly reported.
2 PI3K AKT mTOR growth signaling PI3K/AKT ↓; proliferation ↓; apoptosis ↑ ↔ or stress protection ↑ R, G Growth-signal suppression Most relevant for cinnamaldehyde-rich preparations; linked to colorectal and other cancer models.
3 Mitochondrial apoptosis Bax ↑; Bcl-2 ↓; mitochondrial dysfunction ↑; caspase activation ↑ ↔ at lower exposure; cytotoxicity risk at high exposure G Apoptotic induction Central anticancer mechanism but often requires concentrations above dietary exposure.
4 Glycolysis and HK2 driven invasion HK2 ↓; G6P/F6P production ↓; migration ↓; invasion ↓ ↔ G Anti-metastatic metabolic suppression Mechanistically important for metastatic dissemination models; not a broad direct Warburg enzyme inhibitor claim.
5 VEGF VEGFR2 HIF-1α angiogenesis axis VEGF ↓; HIF-1α ↓; tumor angiogenesis ↓ Angiogenesis ↑ in repair contexts; VEGF-stimulated pathological signaling may be ↓ R, G Context-dependent angiogenesis normalization Direction differs by context: anti-angiogenic in tumor models, but potentially pro-repair in normal tissue wound-healing/endothelial recovery settings.
6 ROS redox stress ROS ↑ and apoptosis ↑ in some tumor models (dose-dependent) ROS ↓ or antioxidant response ↑ at lower exposure P, R Context-dependent redox modulation Not simply antioxidant or pro-oxidant; direction depends on compound, dose, exposure time, and cell stress state.
7 NRF2 antioxidant response NRF2 ↑ may be protective or resistance-relevant (context-dependent) NRF2 ↑; cytoprotective gene expression ↑ R, G Stress-response activation Important safety/normal-cell protection axis; in cancer it may be double-edged if persistent NRF2 supports survival.
8 Cell-cycle regulation G1 or G2/M arrest ↑; cyclin/CDK signaling ↓ ↔ G Cytostasis Secondary to upstream growth and stress signaling changes.
9 MAPK stress signaling JNK/p38 modulation ↑; ERK modulation mixed ↔ or inflammatory MAPK ↓ P, R Signal reprogramming Direction varies by model and stimulus; best treated as contextual rather than primary.
10 Clinical Translation Constraint Systemic exposure uncertain; in-vitro dose gap likely Cassia coumarin hepatotoxicity risk; CYP interaction potential G Translation limitation Ceylon cinnamon is preferred for repeated higher intake because cassia generally has higher coumarin content.

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).



mTOR, mammalian target of rapamycin: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
mTOR (mechanistic target of rapamycin) is a central regulator of cell growth, proliferation, metabolism, and survival. It is a serine/threonine kinase that integrates signals from nutrients, growth factors, and cellular energy status.
mTOR promotes protein synthesis and cell growth by activating downstream targets such as S6 kinase and 4E-BP1. In cancer, this pathway can become hyperactivated, leading to uncontrolled cell proliferation.

mTor Inhibitors:
-rapamycin (Sirolimus): classic natural product mTOR inhibitor
-Curcumin
-Resveratrol
-Epigallocatechin Gallate (EGCG)
-Honokiol
Scientific Papers found: Click to Expand⟱
6163- Cin,    Cinnamaldehyde inhibits the progression of gastric cancer by regulating glycolysis through PTP1B/PI3K/AKT/mTOR signaling pathway
- in-vitro, GC, NA
Glycolysis↓, Cinnamaldehyde inhibits the progression of gastric cancer by regulating glycolysis through PTP1B/PI3K/AKT/mTOR signaling pathway
PI3K↓,
Akt↓,
mTOR↓,

6162- Cin,    Anticancer Potential and Molecular Mechanisms of Cinnamaldehyde and Its Congeners Present in the Cinnamon Plant
- Review, Var, NA
AntiCan↑, Cinnamaldehyde and its congeners have shown their ability to act against several cancers.
Apoptosis↑, graphical abstract
ROS↑,
BAX↑,
Cyt‑c↑,
Fas↑,
Casp9↑,
E-cadherin↑,
Casp7↑,
PARP↑,
Bak↑,
AMPK↑,
Ca+2↑,
BAD↑,
MMP↓,
cycA1/CCNA1↓,
CycB/CCNB1↓,
ERK↓,
VEGF↓,
TumCP↓,
MAPK↓,
mTOR↓,
PI3K↓,
PCNA↓,
Bcl-2↓,
TumCCA↑, Some of the mechanistic approaches include the induction of apoptosis, cell cycle arrest, interruption in angiogenesis, free radical scavenging, inhibition of inflammation, and interference with cellular invasion and metastasis.
angioG↓,
*ROS↓,
Inflam↓,

6141- Cin,    The role and mechanism of cinnamaldehyde in cancer
- Review, Var, NA
Apoptosis↑, Cinnamaldehyde has diverse anti-cancer mechanisms, including inducing apoptosis by activating caspases and damaging mitochondrial function, inhibiting tumor angiogenesis, anti-proliferation, anti-inflammatory and antioxidant.
Casp↑,
mtDam↑,
angioG↓,
TumCP↓,
*Inflam↓,
*antiOx↑,
*ROS↓, In addition, cinnamaldehyde also acts as a reactive oxygen species scavenger, reducing oxidative stress and preventing DNA damage and genomic instability.
*DNAdam↓,
ROS↑, studies have shown that CA can enhance intracellular reactive oxygen species (ROS) levels by inducing mitochondrial dysfunction
*Bcl-2↑, CA exhibits a noteworthy upregulation of B-cell lymphoma protein 2 (Bcl-2) expression (a marker of antiapoptosis), while simultaneously downregulating Bax expression
*BAX↓,
*NF-kB↓, CA has been found to inhibit the activation of nuclear factor-kappa B (NF-κB)
ChemoSen↑, CA enhances the effectiveness of oxaliplatin by promoting apoptosis both in vitro and in vivo
ICAM-1↓, CA down-regulated the expression of adhesion molecules Intercellular adhesion molecule-1 (ICAM-1) and Vascular cell adhesion molecule-1 (VCAM-1)
VCAM-1↓,
PI3K↓, CA downregulates various components of the p PI3K/AKT/mTOR pathway in oral cancer cell lines
Akt↓,
mTOR↓,
BioAv↝, he estimated oral bioavailability of CA was found to be less than 20% for both the 250 and 500 mg/kg doses

6140- Cin,  HCAs,    Cinnamaldehyde: Pharmacokinetics, anticancer properties and therapeutic potential (Review)
- Review, Var, NA
Dose↝, Cinnamaldehyde (CA), an active compound derived from the natural plant cinnamon, has garnered attention in pharmacological research due to its diverse therapeutic applications.
TumCP↓, CA and its derivatives have antitumor effects, which encompass inhibiting cell proliferation, arresting the cell cycle, inducing apoptosis, limiting cell migration and invasion, and suppressing angiogenesis.
TumCCA↑,
Apoptosis↑,
TumCMig↓,
TumCI↓,
angioG↓,
*Inflam↓, including anti-inflammatory (3), antioxidant (4), antiviral (5), anti-bacterial (6), antithrombic (7), hypoglycemic (8), hepatoprotective (9), anti-diabetic (10), neuroprotective (11) and anticancer effects
*antiOx↑,
*Bacteria↓,
*AntiThr↑,
*hepatoP↑,
*AntiDiabetic↑,
*neuroP↑,
AntiCan↑,
ChemoSen↑, can enhance the effectiveness of anticancer drugs and ensure patient safety.
*BioAv↝, the bioavailability of intravenous administration of CA was superior to that of oral administration
*BioAv↑, A into CA solid lipid nanoparticles, which increased the oral bioavailability of CA by >1.69 times.
Synergy↑, Especially when combined with hyperthermia therapy at 42°C and 43°C, CA could inhibit cell proliferation
CDK1↓, CB403 (Fig. 1) is a cinnamaldehyde derivative that inhibits the activity of cyclin-dependent kinases (CDKs), particularly CDK1, CDK2 and CDK4, thereby halting cell cycle progression.
CDK2↓,
CDK4↓,
cJun↓, 2-hydroxycinnamaldehyde (HCA; Fig. 1) inhibits the growth of SW620 colon cancer cells by reducing the expression of c-Jun and c-Fos, inhibiting the DNA binding activity of activator protein 1, and inducing cell apoptosis
cFos↓,
Apoptosis↑,
PI3K↓, CA can induce apoptosis in colon cancer cells by inhibiting the PI3K/Akt signaling pathway
Akt↓,
E-cadherin↑, CA upregulates the expression of E-cadherin while downregulating the expression of matrix metalloproteinase-2 (MMP2) and MMP9
MMP2↓,
MMP9↓,
TOP1↓, increases the sensitivity of CRC cells to 5-FU by reducing the expression of thymidylate synthase, ERCC1, DNA topoisomerase 1 and BRCA1
BRCA1↓,
ROS↑, CA was also able to induce apoptosis in cancer cells by increasing intracellular ROS levels
BAX↑, A induces cell apoptosis by upregulating Bax expression, and downregulating Bcl-2 and X-linked inhibitor of apoptosis (XIAP) expression
Bcl-2↓,
XIAP↓,
MMP↓, CA can also induce apoptosis in leukemia K562 cells by reducing the mitochondrial transmembrane potential via mitochondrial-mediated pathways
STAT3↓, figure 2
mTOR↓,
NF-kB↓, ↓NF-κB
eff↑, CA-Cu-PDA was able to release copper ions and CA in tumor cells, and weakened the antioxidant system by binding to glutathione (GSH), which in turn produced additional ROS, thereby inducing enhanced oxidative stress effects
toxicity↓, Consistent with these findings, another study has demonstrated that CA does not exhibit genotoxic or carcinogenic effects on the body
cardioP↑, CA has demonstrated a capacity to alleviate cardiotoxicity induced by DOX


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 3,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   Glycolysis↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 4,   BAD↑, 1,   Bak↑, 1,   BAX↑, 2,   Bcl-2↓, 2,   Casp↑, 1,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Fas↑, 1,   XIAP↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 3,   ERK↓, 1,   MAPK↓, 1,   mTOR↓, 4,   PI3K↓, 4,   STAT3↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

BRCA1↓, 1,   PARP↑, 1,   PCNA↓, 1,   TOP1↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cFos↓, 1,   TumCP↓, 3,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   E-cadherin↑, 2,   MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 3,   VCAM-1↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

MMP↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ICAM-1↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 2,   Dose↝, 1,   eff↑, 1,   Synergy↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BRCA1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   cardioP↑, 1,   toxicity↓, 1,  
Total Targets: 56

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   ROS↓, 2,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   Bcl-2↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   BioAv↝, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1,   hepatoP↑, 1,   neuroP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 14

Scientific Paper Hit Count for: mTOR, mammalian target of rapamycin
4 Cinnamon
1 Hydroxycinnamic-acid
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#:62  Target#:209  State#:%  Dir#:1
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