Curcumin / AntiAge 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↓, 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


AntiAge, Anti-aging: Click to Expand ⟱
Source:
Type:
Anti-aging strategies hold promise for improving overall health and potentially reducing cancer risk, the intricate interplay between the molecular mechanisms of aging and cancer requires careful consideration.
Scientific Papers found: Click to Expand⟱
5792- CRMs,  HCA,  CUR,  EGCG,  GAR  Caloric restriction mimetics: natural/physiological pharmacological autophagy inducers
- Review, Nor, NA
*CRM↓, *Dose?, *AntiAge↑, *Acetyl-CoA↓, *SIRT1↑, *AMPK↑, *mTORC1↓, *AntiAge↑, chemoP↑,
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↓,
4654- CUR,    Stem Cell Therapy: Curcumin Does the Trick
- Review, Var, NA
*antiOx↑, *Inflam↓, AntiCan↑, chemoPv↑, *AntiAge↑, *neuroP↑, *Wound Healing↑,
4670- RES,  CUR,  EGCG,  TQ,    Targeting aging pathways with natural compounds: a review of curcumin, epigallocatechin gallate, thymoquinone, and resveratrol
- Review, Nor, NA
*antiOx↑, *Inflam↓, *AntiAge↑, *SIRT1↑, *SIRT3↑, *FOXO↑, *ROS↓,

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:


Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   chemoPv↑, 1,  
Total Targets: 3

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   HO-1↑, 1,   lipid-P↓, 1,   MPO↓, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 2,   SIRT3↑, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

Acetyl-CoA↓, 1,   AMPK↑, 2,   CRM↓, 1,   LDL↓, 1,   NADPH↓, 1,   SIRT1↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

FOXO↑, 1,   GSK‐3β↓, 1,   mTOR↓, 1,   mTORC1↓, 1,  

Migration ⓘ

CDK5↓, 1,   TXNIP↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL10↑, 1,   IL17↓, 1,   IL1β↓, 1,   IL23↓, 1,   Inflam↓, 3,   MCP1↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   BDNF↑, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose?, 1,  

Functional Outcomes ⓘ

AntiAge↑, 5,   memory↑, 1,   neuroP↑, 2,   OS↑, 1,   Wound Healing↑, 1,  
Total Targets: 42

Scientific Paper Hit Count for: AntiAge, Anti-aging
4 Curcumin
2 EGCG (Epigallocatechin Gallate)
1 Calorie Restriction Mimetics
1 HydroxyCitric Acid
1 Garcinol
1 Resveratrol
1 Thymoquinone
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#:1245  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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