Curcumin / TNF-α 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↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓">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


TNF-α, TNF-α: Click to Expand ⟱
Source: HalifaxProj (block)
Type:
Tumor Necrosis Factor-alpha (TNF-α) is a cytokine that plays a complex role in cancer biology. It is primarily produced by activated macrophages and is involved in systemic inflammation. TNF-α is a pro-inflammatory cytokine that can promote inflammation, which is a known factor in cancer development.
Overall, the expression of TNF-α in cancers is often linked to inflammation, tumor progression, and the tumor microenvironment.
Scientific Papers found: Click to Expand⟱
3795- CUR,    Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence
- Review, AD, NA
*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↓,
3794- CUR,    Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities
- Review, AD, NA
*GSK‐3β↓, *CDK5↓, *p‑tau↓, *IronCh↑, *ROS↓, *HO-1↑, *SOD↑, *Catalase↑, *GSH↑, *TNF-α↓, *IL6↓, *IL12↓, *NRF2↑, *PPARγ↑, *IL4↑, *AChE↓, *Dose↝, *GutMicro↑,
6050- CUR,  SeNPs,    Efficacy of curcumin-selenium nanoemulsion in alleviating oxidative damage induced by aluminum chloride in a rat model of Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, *AChE↓, *Aβ↓, *P53↓, *tau↓, *NRF2↓, *TNF-α↓, *NO↑, *Catalase↑, *antiOx↑, *Inflam↓,
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, NA
*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↑,
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, NA
*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, NA
*TNF-α↓, *IL1β↓, *NF-kB↓, *PGE2↓, *COX2↓, *MMPs↓, *eff↑,
3581- CUR,    Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer's Disease
- NA, AD, NA
*antiOx↑, *Inflam↓, *BBB↑, *NRF2↑, *NF-kB↓, *cognitive↑, *ROS↓, *MDA↓, *SOD↑, *Catalase↑, *INF-γ↓, *IL4↓, *memory↑, *TNF-α↓, *IL1β↓,
3574- CUR,    The effect of curcumin (turmeric) on Alzheimer's disease: An overview
- Review, AD, NA
*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↑,
1418- CUR,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
*COX2↓, *Inflam↓, *5LO↓, *NO↓, *NF-kB↓, *TNF-α↓, *IL1↓, *IL2↑, *IL6↓, *IL8↓, *IL12↓, *MCP1↓, *PGE2↓, *MMP2↓, *MMP3↓, *MMP9↓, *NLRP3↓, *ROS↓,
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↓,
2133- TQ,  CUR,  Cisplatin,    Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling
- in-vitro, Nor, HEK293 - in-vivo, NA, NA
*creat↓, *TNF-α↓, *IL6↓, *MRP↓, *GFR↑, *mt-ATPase↑, *p‑Akt↑, *NRF2↑, *HO-1↑, *Casp3↓, *NF-kB↓, *RenoP↑,

Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


Mitochondria & Bioenergetics ⓘ

MKP5↑, 1,  

Cell Death ⓘ

p38↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  
Total Targets: 6

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 5,   Catalase↑, 4,   GPx↑, 1,   GSH↑, 3,   GSR↓, 1,   H2O2↓, 1,   HO-1↑, 4,   lipid-P↓, 3,   MDA↓, 2,   MPO↓, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 5,   RNS↓, 1,   ROS↓, 7,   SOD↑, 5,  

Metal & Cofactor Biology ⓘ

IronCh↑, 2,  

Mitochondria & Bioenergetics ⓘ

AIF↓, 1,   ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   LDH↓, 1,   LDL↓, 1,   NADPH↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

p‑Akt↑, 1,   Apoptosis↓, 1,   Casp3↓, 2,   Casp9↓, 1,   iNOS↓, 2,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 3,   mTOR↓, 1,   STAT↓, 1,  

Migration ⓘ

5LO↓, 1,   AP-1↓, 1,   mt-ATPase↑, 1,   CDK5↓, 2,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TXNIP↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 2,   NO↑, 1,  

Barriers & Transport ⓘ

BBB↑, 3,   MRP↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 6,   IL1↓, 2,   IL10↑, 1,   IL12↓, 3,   IL17↓, 1,   IL1β↓, 5,   IL2↓, 2,   IL2↑, 1,   IL23↓, 1,   IL4↓, 2,   IL4↑, 1,   IL6↓, 5,   IL8↓, 2,   INF-γ↓, 2,   Inflam↓, 7,   MCP1↓, 2,   NF-kB↓, 7,   PGE2↓, 3,   TNF-α↓, 10,  

Synaptic & Neurotransmission ⓘ

AChE↓, 3,   BDNF↑, 1,   tau↓, 2,   p‑tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 3,   BACE↓, 1,   NLRP3↓, 2,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

creat↓, 1,   GutMicro↑, 1,   IL6↓, 5,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cardioP↑, 1,   cognitive↑, 5,   cognitive↝, 1,   GFR↑, 1,   memory↑, 4,   neuroP↑, 2,   OS↑, 1,   RenoP↑, 1,   toxicity∅, 1,  
Total Targets: 92

Scientific Paper Hit Count for: TNF-α, TNF-α
11 Curcumin
1 Selenium NanoParticles
1 Resveratrol
1 Ginger/6-Shogaol/Gingerol
1 Thymoquinone
1 Cisplatin
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#:309  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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