Curcumin / LAMs 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


LAMs, Laminins: Click to Expand ⟱
Source:
Type:
Laminins are a family of glycoproteins that play a key role in the structure and function of basement membranes. They are critical for cell differentiation, adhesion, and migration, and these functions have important implications in cancer biology.
-Laminins are major components of the basement membrane—a specialized form of the extracellular matrix (ECM). They provide structural support to tissues and serve as a substrate that influences cell behavior.
-Laminins are composed of three different chains (α, β, and γ), which form a cross-shaped molecule. Different combinations of these chains give rise to various laminin isoforms, each with specific tissue distribution and functions.
-In some studies, cancer cells have been shown to use laminin-rich environments as migratory highways during metastasis. The interaction between laminin and integrins on tumor cells can promote invasive behavior.
-Laminin also plays a role in angiogenesis.
-Enzymes such as matrix metalloproteinases (MMPs) are capable of degrading laminin, and this degradation is often upregulated in cancer. The resulting laminin fragments can have bioactive properties that further modulate tumor progression.
-Laminin-332 (α3β3γ2): Frequently overexpressed in many carcinomas.
-The γ2 chain (LAMC2) in particular is often used as a biomarker for invasive behavior and poor prognosis.
-Contributes to cell adhesion, migration, and invasion due to its interaction with integrins (e.g., α3β1, α6β4).


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↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

HO-1↑, 1,   NQO1↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics

XIAP↓, 1,  

Cell Death

Akt↑, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,  

Kinase & Signal Transduction

SOX9?, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics

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

Autophagy & Lysosomes

LC3II↓, 1,  

DNA Damage & Repair

DNAdam↑, 1,   DNMT1↓, 1,   p16↑, 1,   TP53↑, 1,  

Cell Cycle & Senescence

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State

CSCs↓, 1,   EMT↓, 1,   Nanog↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PTEN↑, 1,   SOX2↓, 1,   STAT3↓, 1,  

Migration

CXCL12↓, 1,   LAMs↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TGF-β↓, 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,  

Clinical Biomarkers

EZH2↓, 1,   IL6↓, 1,   TP53↑, 1,  
Total Targets: 46

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: LAMs, Laminins
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#:1325  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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