Curcumin / LC3II 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


LC3II, Microtubule-associated protein 1A/1B light chain 3: Click to Expand ⟱
Source:
Type:
LC3II (Microtubule-associated protein 1A/1B light chain 3, also known as LC3) is a protein that plays a crucial role in the process of autophagy. Autophagy is a cellular process in which cells recycle and remove damaged or dysfunctional components.
LC3II is often used as a marker for autophagy, as its levels increase during autophagic activity.
LC3II is overexpressed in certain types of cancer, including breast, lung, and colon cancer.
LC3II is also known by other names, including:
    MAP1LC3B (Microtubule-associated protein 1 light chain 3 beta)
    LC3B (Microtubule-associated protein 1 light chain 3 beta)
    ATG8F (Autophagy-related protein 8F)
: In many cancers, increased LC3-II expression indicates enhanced autophagy, which can support tumor cell survival, especially under stress conditions (e.g., nutrient deprivation, hypoxia). This is often associated with poor prognosis and treatment resistance.


Scientific Papers found: Click to Expand⟱
2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, *SOD↑, p16↑, JAK2↓, STAT3↓, CXCL12↓, IL6↓, MMP2↓, MMP9↓, TGF-β↓, α-SMA↓, LAMs↓, DNAdam↑, *memory↑, *cognitive↑, *Inflam↓, *antiOx↑, *NO↑, *MDA↓, *ROS↓, DNMT1↓, ROS↑, Casp3↑, Apoptosis↑, miR-21↓, LC3II↓, ChemoSen↑, NF-kB↓, CSCs↓, Nanog↓, OCT4↓, SOX2↓, eff↑, Sp1/3/4↓, miR-27a-3p↓, ZBTB10↑, SOX9?, ChemoSen↑, VEGF↓, XIAP↓, Bcl-2↓, cycD1/CCND1↓, BioAv↑, Hif1a↓, EMT↓, BioAv↓, PTEN↑, VEGF↓, Akt↑, EZH2↓, NOTCH1↓, TP53↑, NQO1↑, HO-1↑,
457- CUR,    Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling
- in-vitro, GC, SGC-7901 - in-vitro, GC, BGC-823
TumCP↓, Apoptosis↑, TumAuto↑, P53↑, PI3K↓, P21↑, p‑Akt↓, p‑mTOR↓, Bcl-2↓, Bcl-xL↓, LC3I↓, BAX↑, Beclin-1↑, cl‑Casp3↑, cl‑PARP↑, LC3II↑, ATG3↑, ATG5↑,
463- CUR,    Curcumin induces autophagic cell death in human thyroid cancer cells
- in-vitro, Thyroid, K1 - in-vitro, Thyroid, FTC-133 - in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, 8505C
TumAuto↑, LC3II↑, Beclin-1↑, p‑p38↑, p‑JNK↑, p‑ERK↑, p62↓, p‑PDK1↓, p‑Akt↓, p‑p70S6↓, p‑PIK3R1↓, p‑S6↓, p‑4E-BP1↓,
143- CUR,    Nonautophagic cytoplasmic vacuolation death induction in human PC-3M prostate cancer by curcumin through reactive oxygen species -mediated endoplasmic reticulum stress
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ER Stress↑, CHOP↑, GRP78/BiP↑, ROS↑, LC3II↑, eff↓, tumCV↓,

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

HO-1↑, 1,   NQO1↑, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics

XIAP↓, 1,  

Core Metabolism/Glycolysis

p‑PDK1↓, 1,   p‑PIK3R1↓, 1,   p‑S6↓, 1,  

Cell Death

Akt↑, 1,   p‑Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   p‑JNK↑, 1,   p‑p38↑, 1,  

Kinase & Signal Transduction

p‑p70S6↓, 1,   SOX9?, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics

EZH2↓, 1,   miR-21↓, 1,   miR-27a-3p↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress

CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,  

Autophagy & Lysosomes

ATG3↑, 1,   ATG5↑, 1,   Beclin-1↑, 2,   LC3I↓, 1,   LC3II↓, 1,   LC3II↑, 3,   p62↓, 1,   TumAuto↑, 2,  

DNA Damage & Repair

DNAdam↑, 1,   DNMT1↓, 1,   p16↑, 1,   P53↑, 1,   cl‑PARP↑, 1,   TP53↑, 1,  

Cell Cycle & Senescence

cycD1/CCND1↓, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State

p‑4E-BP1↓, 1,   CSCs↓, 1,   EMT↓, 1,   p‑ERK↑, 1,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PI3K↓, 1,   PTEN↑, 1,   SOX2↓, 1,   STAT3↓, 1,  

Migration

CXCL12↓, 1,   LAMs↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TGF-β↓, 1,   TumCP↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature

Hif1a↓, 1,   VEGF↓, 2,   ZBTB10↑, 1,  

Immune & Inflammatory Signaling

IL6↓, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 2,   eff↓, 1,   eff↑, 1,  

Clinical Biomarkers

EZH2↓, 1,   IL6↓, 1,   TP53↑, 1,  
Total Targets: 76

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   MDA↓, 1,   ROS↓, 2,   SOD↑, 1,  

Angiogenesis & Vasculature

NO↑, 1,  

Immune & Inflammatory Signaling

Inflam↓, 1,  

Functional Outcomes

cognitive↑, 1,   memory↑, 1,  
Total Targets: 8

Scientific Paper Hit Count for: LC3II, Microtubule-associated protein 1A/1B light chain 3
4 Curcumin
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#:721  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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