Ferulic acid / COX2 Cancer Research Results

FA, Ferulic acid: Click to Expand ⟱
Features:
Ferulic acid is an antioxidant found in some skin creams and serums.
Foods: popcorn, bamboo, whole-grain rye bread, whole-grain oat flakes, sweet corn (cooked)
Ferulic acid (FA) is a hydroxycinnamic acid abundant in plant cell walls (notably cereals/whole grains) with strong antioxidant and cytoprotective activity. Mechanistically, FA is frequently described as inducing Nrf2/HO-1 antioxidant programs and suppressing NF-κB-linked inflammation, with additional model-dependent anticancer effects (cell-cycle arrest, apoptosis, reduced invasion). Oral exposure is variable because FA is rapidly metabolized (often as conjugates) and bioaccessibility depends on the food matrix.

-Ferulic acid found in dietary strand fractions, especially its free form, has important functions for protecting the human health.
-AChE inhibitor (AD)
-Cooking results in an increase in free ferulic acid quantity and in a reduction in bound ferulic acid quantity.
Bamboo shoots       243.6 mg/100g
Sugar-beet pulp     800 mg/100g
Popcorn             313 mg/100g
Wheat bran	    500–1500mg/100g
Whole wheat flour   100–300mg/100g
            
Type of corn p-coumaric acidferulic acid
   mg/kg, DW mg/kg, DW
Yellow dent 18.9 265
American blue N.D. 927
Mexican blue 1.3 202
white 6.6 2484
Pathway / Target	Modulation by FA / Direction
Aβ aggregation	         ↓ Inhibits fibril formation and destabilizes existing Aβ fibrils 
BACE‑1 & APP	         ↓ Reduces BACE-1 and APP expression; ↑ MMP‑2/‑9 expression promoting Aβ clearance
Tau hyperphosphorylation  Implicitly ↓ through modulation of Ca²⁺/CDK5/GSK3β pathways
Ca²⁺         	         ↓ FA lowers STEP levels via chelation of Ca²⁺, suppressing PP2B → restores synaptic plasticity
(AChE / BChE)	         ↓ Inhibition of AChE (FA IC₅₀~15 µM, derivatives IC₅₀ down to 0.006 µM); also BChE
(MAO‑A/B)	         ↓ Inhibits MAO‑B (derivatives IC₅₀ ~0.3–0.7 µM), reducing ROS
ROS                      ↓ Scavenges ROS, enhances antioxidant enzymes (e.g., catalase), ↓ MDA
(COX‑2, 5‑LOX, NLRP3)	 ↓ Derivatives inhibit COX‑2/5‑LOX; derivative 13a ↓ NLRP3 inflammasome
Iron/Cu²⁺ chelation	 ↓ Metal-induced Aβ aggregation via chelation by FA and derivatives
Autophagy & Aβ clearance  ↗ Suggested promotion of autophagy mechanisms targeting Aβ
Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Nrf2 → HO-1 / ARE antioxidant response Stress adaptation modulation (context-dependent) Nrf2 ↑; HO-1 ↑; antioxidant defenses ↑ R, G Endogenous antioxidant upshift FA is repeatedly reported to promote Nrf2 nuclear translocation and HO-1 induction; this is one of the most defensible “core” mechanisms.
2 NF-κB inflammatory transcription (COX-2 / iNOS / cytokines) NF-κB ↓; COX-2/iNOS and pro-inflammatory cytokine programs ↓ (reported) Inflammation tone ↓ (tissue protective) R, G Anti-inflammatory signaling Often described as downstream of redox changes and upstream of reduced inflammatory mediators; direction is consistent across many inflammation models.
3 ROS / oxidative stress tone Oxidative stress ↓ (often); ROS direction can vary by tumor model Oxidative injury ↓ P, R, G Redox buffering (context-dependent) FA is classically antioxidant; in tumor systems, effects may be secondary to signaling changes and vary with baseline redox instability.
4 Cell-cycle control (Cyclin D1 / CDK4/6; checkpoints) Cell-cycle arrest ↑ (reported); Cyclin D1 ↓; proliferation ↓ ↔ G Cytostasis Frequently reported as later phenotype-level outcomes; direction and checkpoint phase (G1 vs G2/M) vary by model.
5 Apoptosis (intrinsic caspase-linked; p53 axis in some models) Apoptosis ↑; caspase activation ↑ (reported); p53/p21 ↑ (model-dependent) ↔ (generally less activation) G Cell death execution Apoptosis is commonly observed in cancer models but is not as “signature-direct” as for mitochondrial toxins; best treated as downstream/conditional.
6 MAPK re-wiring (ERK / JNK / p38) MAPK modulation (context-dependent) ↔ P, R, G Signal reprogramming MAPK direction depends on whether FA is acting primarily as anti-inflammatory/anti-stress vs antiproliferative; avoid hard arrows for p38/JNK/ERK unless model-specific.
7 PI3K → AKT (± mTOR) survival axis PI3K/AKT modulation (reported; model-dependent) ↔ R, G Survival/growth modulation Often listed in anticancer summaries; treat as “reported” rather than universal primary mechanism.
8 Invasion / metastasis programs (MMPs / migration) MMPs ↓; migration/invasion ↓ (reported) ↔ G Anti-invasive phenotype Observed as later outcomes (gene expression + phenotype assays) and commonly linked to NF-κB/MAPK context.
9 Radiation/chemo injury mitigation (supportive care framing) Adjunct potential: may reduce treatment-associated oxidative/inflammatory injury (context) Tissue protection ↑ (reported) G Cytoprotection Animal models report radioprotective/anti-inflammatory effects; present as supportive/adjunct rather than standalone anticancer therapy.
10 Bioavailability / metabolism constraint (conjugation; food-matrix dependence) Systemic exposure variable; much appears as glucuronide/sulfate conjugates — — Translation constraint FA is absorbed and rapidly metabolized; “bioavailability” varies widely with food matrix and binding to polysaccharides in grains.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (primary/rapid effects; early redox interactions / rapid signaling shifts)
  • R: 30 min–3 hr (acute stress-response + transcription signaling shifts)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
COX2, cycloocygenase-2 (Cox-2) mRNA and Cox-2 protein: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Cyclooxygenase-2 (COX-2) is an enzyme that plays a critical role in the conversion of arachidonic acid to prostaglandins, which are lipid compounds involved in various physiological processes, including inflammation, pain, and fever. COX-2 is an inducible enzyme, meaning its expression is typically low in normal tissues but can be upregulated in response to inflammatory stimuli, growth factors, and certain oncogenic signals.
-Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin biosynthesis, plays a key role in inflammation and circulatory homeostasis.
-COX-2 is an inducible enzyme that is upregulated in response to pro-inflammatory signals, including cytokines (e.g., IL-1β, TNF-α) and growth factors.

COX-2 is often overexpressed in various tumors, including colorectal, breast, lung, and prostate cancers.
The prostaglandins produced by COX-2, particularly prostaglandin E2 (PGE2), have several effects that can facilitate cancer progression:
Cell Proliferation: PGE2 can promote the proliferation of cancer cells by activating signaling pathways such as the PI3K/Akt and MAPK pathways.
Nonselective NSAIDs, such as aspirin and ibuprofen, inhibit both COX-1 and COX-2. Epidemiological studies have suggested that regular use of NSAIDs may reduce the risk of certain cancers, particularly colorectal cancer.
Drugs specifically targeting COX-2, such as celecoxib, have been developed.

COX-2 and xanthine oxidase are ROS-producing pro-oxidant enzymes that contribute to inflammation. Elevated COX‑2 levels, often found in inflammatory conditions or certain types of cancers, can contribute to increased production of ROS.
Scientific Papers found: Click to Expand⟱
3779- FA,    A review on ferulic acid and analogs based scaffolds for the management of Alzheimer’s disease
- Review, AD, NA
*antiOx↑, *neuroP↑, *Aβ↓, *Inflam↓, *COX2↓, *Casp↓, *NOS2↓, *HO-1↑, *AChE∅, *BChE∅, *memory↑,
3778- FA,    Recent Advances in the Neuroprotective Properties of Ferulic Acid in Alzheimer’s Disease: A Narrative Review
- Review, AD, NA
*neuroP↑, *Aβ↓, *antiOx↑, *Inflam↓, *ROS↓, *NF-kB↓, *NLRP3↓, *iNOS↓, *COX2↓, *TNF-α↓, *IL1β↓, *VCAM-1↓, *ICAM-1↓, *p‑MAPK?, *hepatoP↑, *TLR4↓, *PPARγ↑, *NRF2↑, *Fenton↓, *IronCh↑, *MDA↓, *HO-1↑, *Bil↑, *GCLC↑, *GCLM↑, *NQO1↑, *GutMicro↑, *SOD↑, *Ca+2↓, *lipid-P↓, *PGE2↓,
3714- FA,    Recent Advances in the Neuroprotective Properties of Ferulic Acid in Alzheimer's Disease: A Narrative Review
- Review, AD, NA
*antiOx↑, *Inflam↓, *neuroP↑, *NF-kB↓, *NLRP3↓, *iNOS↓, *COX2↓, *TNF-α↓, *IL1β↓, *VCAM-1↓, *ICAM-1↓, *p‑MAPK↓, *p38↓, *JNK↓, *IL6↓, *IL8↓, *hepatoP↑, *RenoP↑, *Catalase↑, *PPARγ↑, *ROS↓, *Fenton↓, *IronCh↑, *SOD↑, *MDA↓, *lipid-P↓, *NRF2↑, *HO-1↑, *ARE↑, *Bil↑, *radioP↑, *GCLC↑, *GCLM↑, *NQO1↑, *Half-Life↝, *GutMicro↑, *Aβ↓, *BDNF↑, *Ca+2↓, *lipid-P↓, *PGE2↓, *cognitive↑, *ChAT↑, *memory↑, *Dose↝, *toxicity↓,
3712- FA,    Ferulic Acid: A Hope for Alzheimer’s Disease Therapy from Plants
- Review, AD, NA
*antiOx↑, *Inflam↓, *ROS↓, *Aβ↓, *HO-1↑, *HSP70/HSPA5↑, *ERK↑, *Akt↑, *iNOS↓, *COX2↓, *cardioP↑, *memory↑, *IL2↓, *cognitive↑, *APP↓, *SOD↑, *Catalase↑, *Akt↑, *BioAv↑,
1656- FA,    Ferulic Acid: A Natural Phenol That Inhibits Neoplastic Events through Modulation of Oncogenic Signaling
- Review, Var, NA
tyrosinase↓, CK2↓, TumCP↓, TumCMig↓, FGF↓, FGFR1↓, PI3K↓, Akt↓, VEGF↓, FGFR1↓, FGFR2↓, PDGF↓, ALAT↓, AST↓, TumCCA↑, CDK2↓, CDK4↓, CDK6↓, BAX↓, Bcl-2↓, MMP2↓, MMP9↓, P53↑, PARP↑, PUMA↑, NOXA↑, Casp3↑, Casp9↑, TIMP1↑, lipid-P↑, mtDam↑, EMT↓, Vim↓, E-cadherin↓, p‑STAT3↓, COX2↓, CDC25↓, RadioS↑, ROS↑, DNAdam↑, γH2AX↑, PTEN↑, LC3II↓, Beclin-1↓, SOD↓, Catalase↓, GPx↓, Fas↑, *BioAv↓, cMyc↓, Beclin-1↑, LC3‑Ⅱ/LC3‑Ⅰ↓,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↓, 1,   GPx↓, 1,   lipid-P↑, 1,   ROS↑, 1,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 1,   FGFR1↓, 2,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   cMyc↓, 1,  

Cell Death ⓘ

Akt↓, 1,   BAX↓, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   CK2↓, 1,   Fas↑, 1,   NOXA↑, 1,   PUMA↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,   Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↓, 1,   LC3II↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   PARP↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   FGF↓, 1,   FGFR2↓, 1,   PI3K↓, 1,   PTEN↑, 1,   p‑STAT3↓, 1,   tyrosinase↓, 1,  

Migration ⓘ

E-cadherin↓, 1,   MMP2↓, 1,   MMP9↓, 1,   PDGF↓, 1,   TIMP1↑, 1,   TumCMig↓, 1,   TumCP↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

RadioS↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 4,   ARE↑, 1,   Bil↑, 2,   Catalase↑, 2,   Fenton↓, 2,   GCLC↑, 2,   GCLM↑, 2,   HO-1↑, 4,   lipid-P↓, 3,   MDA↓, 2,   NQO1↑, 2,   NRF2↑, 2,   ROS↓, 3,   SOD↑, 3,  

Metal & Cofactor Biology ⓘ

IronCh↑, 2,  

Core Metabolism/Glycolysis ⓘ

PPARγ↑, 2,  

Cell Death ⓘ

Akt↑, 2,   Casp↓, 1,   iNOS↓, 3,   JNK↓, 1,   p‑MAPK?, 1,   p‑MAPK↓, 1,   p38↓, 1,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,  

Migration ⓘ

APP↓, 1,   Ca+2↓, 2,   VCAM-1↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 4,   ICAM-1↓, 2,   IL1β↓, 2,   IL2↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 4,   NF-kB↓, 2,   PGE2↓, 2,   TLR4↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

AChE∅, 1,   BChE∅, 1,   BDNF↑, 1,   ChAT↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 4,   NLRP3↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↝, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

Bil↑, 2,   GutMicro↑, 2,   IL6↓, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 2,   hepatoP↑, 2,   memory↑, 3,   neuroP↑, 3,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 61

Scientific Paper Hit Count for: COX2, cycloocygenase-2 (Cox-2) mRNA and Cox-2 protein
5 Ferulic 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#:77  Target#:66  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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