Curcumin / COX2 Cancer Research Results

CUR, Curcumin: Click to Expand ⟱

Features:

Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown
-may suppress CSC: suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).
Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
curcumin can act as a pro-oxidant when blue light is applied
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓">COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank	Pathway / Axis	Cancer Cells	Normal Cells	Label	Primary Interpretation	Notes
1	NF-κB signaling	↓ NF-κB activation	↓ inflammatory NF-κB tone	Driver	Suppression of survival and inflammatory transcription	NF-κB is a primary, repeatedly validated curcumin target explaining pleiotropic downstream effects
2	STAT3 signaling	↓ STAT3 phosphorylation / activity	↔ or mild suppression	Driver	Loss of pro-survival and proliferative signaling	STAT3 inhibition contributes to growth arrest, apoptosis sensitization, and reduced cytokine signaling in tumors
3	Reactive oxygen species (ROS)	↑ ROS (dose- & context-dependent)	↓ ROS / buffered	Conditional Driver	Biphasic redox modulation	Curcumin can act as a pro-oxidant in cancer cells with high basal stress while acting antioxidant in normal cells
4	Mitochondrial integrity / intrinsic apoptosis	↓ ΔΨm; ↑ caspase activation	↔ preserved	Driver	Execution of intrinsic apoptosis	Mitochondrial dysfunction and caspase activation occur downstream of NF-κB/STAT3 and ROS effects
5	PI3K → AKT → mTOR axis	↓ AKT / ↓ mTOR	↔ or adaptive suppression	Secondary	Reduced growth and anabolic signaling	AKT/mTOR inhibition contributes to growth suppression and autophagy induction in cancer cells
6	Autophagy	↑ autophagy (protective or pro-death)	↑ adaptive autophagy	Secondary	Stress adaptation vs cell death	Autophagy may be cytoprotective or cooperate with apoptosis depending on context and dose
7	HIF-1α / VEGF hypoxia–angiogenesis axis	↓ HIF-1α; ↓ VEGF	↔ minimal effect	Secondary	Anti-angiogenic pressure	Suppression of hypoxia-driven transcription limits angiogenesis and tumor adaptation
8	Cell cycle regulation	↑ G2/M or G1 arrest	↔ largely spared	Phenotypic	Cytostatic growth control	Cell-cycle arrest reflects upstream signaling and epigenetic effects rather than direct CDK inhibition
9	Migration / invasion (EMT, MMP axis)	↓ migration & invasion	↔	Phenotypic	Anti-metastatic phenotype	Reduced EMT markers and protease activity limit invasive behavior
10	Epigenetic regulation (p300/CBP HAT activity)	↓ histone acetylation	↔ modest	Secondary	Transcriptional reprogramming	Curcumin modulates chromatin via HAT inhibition rather than classic HDAC inhibition

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⟱

3795-

CUR,

Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence

Review,

AD,

*antiOx↑, *Inflam↓, *AntiAge↑, *AMPK↑, *SIRT1↑, *NF-kB↓, *mTOR↓, *NLRP3↓, *NADPH↓, *ROS↓, *COX2↓, *MCP1↓, *IL1β↓, *IL17↓, *IL23↓, *TNF-α↓, *MPO↓, *IL10↑, *lipid-P↓, *SOD↑, *Aβ↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓, *TXNIP↓, *NRF2↑, *NQO1↑, *HO-1↑, *OS↑, *memory↑, *BDNF↑, *neuroP↑, *BACE↓, *AChE↓, *LDL↓,

2818-

CUR,

Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways

Review,

AD,

*neuroP↑, *ROS↓, *Inflam↓, *Apoptosis↓, *cognitive↑, *cardioP↑, other↑, *COX2↓, *IL1β↓, *TNF-α↓, NF-kB↓, *PGE2↓, *iNOS↓, *NO↓, *IL2↓, *IL4↓, *IL6↓, *INF-γ↓, *GSK‐3β↓, *STAT↓, *GSH↑, *MDA↓, *lipid-P↓, *SOD↑, *GPx↑, *Catalase↑, *GSR↓, *LDH↓, *H2O2↓, *Casp3↓, *Casp9↓, *NRF2↑, *AIF↓, *ATP↑,

2814-

CUR,

Curcumin in Cancer and Inflammation: An In-Depth Exploration of Molecular Interactions, Therapeutic Potentials, and the Role in Disease Management

Review,

Var,

*BioAv↓, *Inflam↓, *antiOx↑, AntiCan↑, CK2↓, GSK‐3β↓, EGFR↓, TOP1↓, TOP2↓, NF-kB↓, COX2↓, CRP↓,

2466-

CUR,

Regulatory Effects of Curcumin on Platelets: An Update and Future Directions

Review,

Nor,

*AntiAg↑, *antiOx↑, *Inflam↓, *12LOX↑, COX1↓, COX2↓, MMP9↓, NF-kB↓,

3588-

CUR,

The effect of curcumin on cognition in Alzheimer’s disease and healthy aging: A systematic review of pre-clinical and clinical studies

Review,

AD,

*cognitive↝, *BioAv↑, *Inflam↓, *COX2↓, *iNOS↓, *NF-kB↓, *TNF-α↓, *IL1↓, *IL2↓, *IL6↓, *IL8↓, *IL12↓, *ROS↓, *RNS↓, *antiOx↑, *BBB↑, *BioAv↓, *cognitive↑, *memory↑, *tau↓, *eff↑,

3583-

CUR,

Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers

Review,

Arthritis,

*TNF-α↓, *IL1β↓, *NF-kB↓, *PGE2↓, *COX2↓, *MMPs↓, *eff↑,

3574-

CUR,

The effect of curcumin (turmeric) on Alzheimer's disease: An overview

Review,

AD,

*antiOx↑, *Inflam↓, *lipid-P↓, *cognitive↑, *memory↑, *Aβ↓, *COX2↓, *ROS↓, *AP-1↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *SOD↑, *GSH↑, *HO-1↑, *IronCh↑, *BioAv↓, *Half-Life↝, *Dose↝, *BBB↑, *BioAv↑, *toxicity∅, *eff↑,

465-

CUR,

Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor cells in murine tumor tissues

vitro+vivo,

Liver,

HepG2

1.2, 2.4, 4.8 and 9.6 µg/mL, 24 and 48 h; 120 and 240 mg/kg/day, 15 days

vitro+vivo,

Liver,

HUH7

vitro+vivo,

Liver,

MHCC-97H

TumCG↓, MDSCs↓, TLR4↓, NF-kB↓, IL6↓, IL1↓, PGE2↓, COX2↓, GM-CSF↓, angioG↓, VEGF↓, CD31↓, GM-CSF↓, α-SMA↓, p‑IKKα↓, MyD88↓,

1418-

CUR,

Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis

Review,

Arthritis,

*COX2↓, *Inflam↓, *5LO↓, *NO↓, *NF-kB↓, *TNF-α↓, *IL1↓, *IL2↑, *IL6↓, *IL8↓, *IL12↓, *MCP1↓, *PGE2↓, *MMP2↓, *MMP3↓, *MMP9↓, *NLRP3↓, *ROS↓,

1485-

CUR,

Chemo,

Rad,

Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs

Review,

Var,

ChemoSen↑, NF-kB↓, *STAT3↓, *COX2↓, *Akt↓, *NRF2↑, *HO-1↑, *GPx↑, *NADPH↑, *GSH↑, *ROS↓, *p300↓, radioP↑, chemoP↑, RadioS↑,

1792-

CUR,

LEC,

Chondroprotective effect of curcumin and lecithin complex in human chondrocytes stimulated by IL-1β via an anti-inflammatory mechanism

in-vitro,

Arthritis,

RAW264.7

0.5-20 μM as curcumin) and LPS (1 μg/mL) for 48 h.

NA,

HCC-38

*Inflam↓, *NF-kB↓, *iNOS↓, *COX2↓, *NO↓, *PGE2↓, *MMPs↑, *TIMP1↑, *BioEnh↑,

1809-

CUR,

Oxy,

Long-term stabilisation of myeloma with curcumin

Case Report,

Melanoma,

*OS↑, QoL↑, Dose↑, Dose↑, IL6↓, STAT3↓, NF-kB↓, COX2↓,

136-

CUR,

docx,

Combinatorial effect of curcumin with docetaxel modulates apoptotic and cell survival molecules in prostate cancer

in-vitro,

Pca,

DU145

 5-50uM

 19.2 nM(docx), 32.3 μM(CUR)

20 μM curcumin and 10 nM docetaxel significantly decrease (2.7 fold) the proliferation

in-vitro,

Pca,

PC3

 46 nM(docx), 36.1 μM(CUR)

combined treatment decrease (3.2 fold)

Bcl-2↓, Bcl-xL↓, Mcl-1↓, BAX↑, BID↑, PARP↑, NF-kB↓, CDK1↓, COX2↓, RTK-RAS↓, PI3K/Akt↓, EGFR↓, HER2/EBBR2↓, P53↑, ChemoSen↑,

13-

CUR,

Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action

Review,

BC,

P53↑, DR5↑, JNK↑, NRF2↑, PPARγ↑, HER2/EBBR2↓, IR↓, ER(estro)↓, Fas↑, PDGF↓, TGF-β↓, FGF↓, EGFR↓, JAK↓, PAK↓, MAPK↓, ATPase↓, COX2↓, MMPs↓, IL1↓, IL2↓, IL5↓, IL6↓, IL8↓, IL12↓, IL18↓, NF-kB↓, NOTCH1↓, STAT1↓, STAT4↓, STAT5↓, STAT3↓,

182-

CUR,

RES,

GI,

Chemopreventive anti-inflammatory activities of curcumin and other phytochemicals mediated by MAP kinase phosphatase-5 in prostate cells

in-vitro,

Pca,

DU145

in-vitro,

Pca,

PC3

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

LAPC-4

p38↓, MKP5↑, TNF-α↓, COX2↓, NF-kB↓,

158-

CUR,

Curcumin-targeting pericellular serine protease matriptase role in suppression of prostate cancer cell invasion, tumor growth, and metastasis

vitro+vivo,

Pca,

LNCaP

in-vitro,

Pca,

PC3

MMP9↓, Matr↓, Inflam↓, antiOx↓, NF-kB↓, COX2↓, iNOS↓, TumCMig↓, TumCI↓,

160-

CUR,

Curcumin inhibits prostate cancer metastasis in vivo by targeting the inflammatory cytokines CXCL1 and -2

in-vitro,

Pca,

CXCc↓, IκB↓, NF-kB↓, COX2↓, SPARC↓, EFEMP↓, IKKα↓,

Showing Research Papers: 1 to 17 of 17

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 5, Catalase↑, 1, GPx↑, 2, GSH↑, 3, GSR↓, 1, H2O2↓, 1, HO-1↑, 3, lipid-P↓, 3, MDA↓, 1, MPO↓, 1, NQO1↑, 1, NRF2↑, 3, RNS↓, 1, ROS↓, 6, SOD↑, 3,

Metal & Cofactor Biology ⓘ

IronCh↑, 1,

Mitochondria & Bioenergetics ⓘ

AIF↓, 1, ATP↑, 1,

Core Metabolism/Glycolysis ⓘ

12LOX↑, 1, AMPK↑, 1, LDH↓, 1, LDL↓, 1, NADPH↓, 1, NADPH↑, 1, SIRT1↑, 1,

Cell Death ⓘ

Akt↓, 1, Apoptosis↓, 1, Casp3↓, 1, Casp9↓, 1, iNOS↓, 3,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 2, mTOR↓, 1, p300↓, 1, STAT↓, 1, STAT3↓, 1,

Migration ⓘ

5LO↓, 1, AntiAg↑, 1, AP-1↓, 1, CDK5↓, 1, MMP2↓, 1, MMP3↓, 1, MMP9↓, 1, MMPs↓, 1, MMPs↑, 1, TIMP1↑, 1, TXNIP↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 3,

Barriers & Transport ⓘ

BBB↑, 2,

Immune & Inflammatory Signaling ⓘ

COX2↓, 8, IL1↓, 2, IL10↑, 1, IL12↓, 2, IL17↓, 1, IL1β↓, 4, IL2↓, 2, IL2↑, 1, IL23↓, 1, IL4↓, 1, IL6↓, 3, IL8↓, 2, INF-γ↓, 1, Inflam↓, 8, MCP1↓, 2, NF-kB↓, 6, PGE2↓, 4, TNF-α↓, 6,

Synaptic & Neurotransmission ⓘ

AChE↓, 1, BDNF↑, 1, tau↓, 1, p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 2, BACE↓, 1, NLRP3↓, 2,

Drug Metabolism & Resistance ⓘ

BioAv↓, 3, BioAv↑, 2, BioEnh↑, 1, Dose↝, 1, eff↑, 3, Half-Life↝, 1,

Clinical Biomarkers ⓘ

IL6↓, 3, LDH↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, cardioP↑, 1, cognitive↑, 3, cognitive↝, 1, memory↑, 3, neuroP↑, 2, OS↑, 2, toxicity∅, 1,
Total Targets: 89

Scientific Paper Hit Count for: COX2, cycloocygenase-2 (Cox-2) mRNA and Cox-2 protein

17 Curcumin
1 Chemotherapy
1 Radiotherapy/Radiation
1 Lecithin
1 Oxygen, Hyperbaric
1 Docetaxel
1 Resveratrol
1 Ginger/6-Shogaol/Gingerol

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#:65  Target#:66  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

Curcumin / COX2 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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