Luteolin / E-cadherin Cancer Research Results

LT, Luteolin: Click to Expand ⟱
Features:
Luteolin a Flavonoid found in celery, parsley, broccoli, onion leaves, carrots, peppers, cabbages, apple skins, and chrysanthemum flowers.
-MDR1 expression, MMP-9, IGF-1 and Epithelial to mesenchymal transition.

-Note half-life 2–3 hours
BioAv low, but could be improved with Res, or blend of castor oil, kolliphor and polyethylene glycol
Pathways:
- induce ROS production in cancer cell but a few reports of reduction. Always seems to reduce ROS in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, LDHA↓, HK2↓, GRP78↑,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, TrxR**, - Shown to modulate the nuclear translocation of SREBP-2 (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Luteolin — Cancer vs Normal Cell Effects
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR signaling ↔ adaptive suppression Driver Loss of survival and growth signaling Luteolin consistently suppresses PI3K/AKT signaling, explaining growth inhibition and apoptosis sensitization
2 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Driver Suppression of inflammatory survival transcription NF-κB inhibition is a core, repeatedly observed luteolin effect
3 Reactive oxygen species (ROS) ↑ ROS (context- & dose-dependent) ↓ ROS / buffered Conditional Driver Biphasic redox modulation Luteolin can act as a pro-oxidant in cancer cells while remaining antioxidant in normal cells
4 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Secondary Execution of intrinsic apoptosis Mitochondrial apoptosis follows signaling and redox stress
5 STAT3 signaling ↓ STAT3 activation ↔ minimal Secondary Loss of proliferative and stemness signaling STAT3 suppression contributes to reduced invasion and CSC traits
6 Cell cycle regulation ↑ G1 or G2/M arrest ↔ spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects upstream pathway inhibition
7 Migration / invasion (EMT, MMP axis) ↓ migration & invasion Phenotypic Anti-metastatic phenotype Reduced EMT and protease activity limit invasiveness


E-cadherin, E-cadherin: Click to Expand ⟱
Source: HalifaxProj(restore)
Type:
Also known as Cadherin1 (CDH1)
E-cadherin, is a type of cell adhesion molecule that plays a crucial role in maintaining tissue structure and cell-cell interactions. In the context of cancer, E-cadherin has been found to be a tumor suppressor gene.

E-cadherin is a transmembrane protein that mediates cell-cell adhesion through its extracellular domain, which interacts with other E-cadherin molecules on adjacent cells. This interaction helps to maintain tissue integrity and prevent cancer cells from invading surrounding tissues.

In many types of cancer, including breast, colon, and prostate cancer, E-cadherin expression is often reduced or lost.
cell adhesion molecules spanning four families of 1) Integrins (α2β1, α5/β1, αL/β2); 2) Cadherins (E-cad, P-cad, N-cad); 3) Ig-CAMs (VCAM, NCAM, ICAM, Nectins, Necl); and 4) Selectins (E-selectin, P-selectin, L-selectin).


Scientific Papers found: Click to Expand⟱
2916- LT,    Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies
- Review, Var, NA - Review, AD, NA - Review, Park, NA
proCasp9↓, CDC2↓, CycB/CCNB1↓, Casp9↑, Casp3↑, Cyt‑c↑, cycA1/CCNA1↑, CDK2↓, APAF1↑, TumCCA↑, P53↑, BAX↑, VEGF↓, Bcl-2↓, Apoptosis↑, p‑Akt↓, p‑EGFR↓, p‑ERK↓, p‑STAT3↓, cardioP↑, Catalase↓, SOD↓, *BioAv↓, *antiOx↑, *ROS↓, *NO↓, *GSTs↑, *GSR↑, *SOD↑, *Catalase↑, *lipid-P↓, PI3K↓, Akt↓, CDK2↓, BNIP3↑, hTERT/TERT↓, DR5↑, Beclin-1↑, TNF-α↓, NF-kB↓, IL1↓, IL6↓, EMT↓, FAK↓, E-cadherin↑, MDM2↓, NOTCH↓, MAPK↑, Vim↓, N-cadherin↓, Snail↓, MMP2↓, Twist↓, MMP9↓, ROS↑, MMP↓, *AChE↓, *MMP↑, *Aβ↓, *neuroP↑, Trx1↑, ROS↓, *NRF2↑, NRF2↓, *BBB↑, ChemoSen↑, GutMicro↑,
2914- LT,    Therapeutic Potential of Luteolin on Cancer
- Review, Var, NA
*antiOx↑, *IronCh↑, *toxicity↓, *BioAv↓, *BioAv↑, DNAdam↑, TumCP↓, DR5↑, P53↑, JNK↑, BAX↑, cl‑Casp3↑, cl‑Casp8↑, cl‑Casp9↑, cl‑PARP↑, survivin↓, cycD1/CCND1↓, CycB/CCNB1↓, CDC2↓, P21↑, angioG↓, MMP2↓, AEG1↓, VEGF↓, VEGFR2↓, MMP9↓, CXCR4↓, PI3K↓, Akt↓, ERK↓, TumAuto↑, LC3B-II↑, EMT↓, E-cadherin↑, N-cadherin↓, Wnt↓, ROS↑, NICD↓, p‑GSK‐3β↓, iNOS↓, COX2↓, NRF2↑, Ca+2↑, ChemoSen↑, ChemoSen↓, IFN-γ↓, RadioS↑, MDM2↓, NOTCH1↓, AR↓, TIMP1↑, TIMP2↑, ER Stress↑, CDK2↓, Telomerase↓, p‑NF-kB↑, p‑cMyc↑, hTERT/TERT↓, RAS↓, YAP/TEAD↓, TAZ↓, NF-kB↓, NRF2↓, HO-1↓, MDR1↓,
2912- LT,    Luteolin: a flavonoid with a multifaceted anticancer potential
- Review, Var, NA
ROS↑, TumCCA↑, TumCP↓, angioG↓, ER Stress↑, mtDam↑, PERK↑, ATF4↑, eIF2α↑, cl‑Casp12↑, EMT↓, E-cadherin↑, N-cadherin↓, Vim↓, *neuroP↑, NF-kB↓, PI3K↓, Akt↑, XIAP↓, MMP↓, Ca+2↑, BAX↑, Casp3↑, Casp9↑, Bcl-2↓, Cyt‑c↑, IronCh↑, SOD↓, *ROS↓, *LDHA↑, *SOD↑, *GSH↑, *BioAv↓, Telomerase↓, cMyc↓, hTERT/TERT↓, DR5↑, Fas↑, FADD↑, BAD↑, BOK↑, BID↑, NAIP↓, Mcl-1↓, CDK2↓, CDK4↓, MAPK↓, AKT1↓, Akt2↓, *Beclin-1↓, Hif1a↓, LC3II↑, Beclin-1↑,
2927- LT,    Luteolin Causes 5′CpG Demethylation of the Promoters of TSGs and Modulates the Aberrant Histone Modifications, Restoring the Expression of TSGs in Human Cancer Cells
- in-vitro, Cerv, HeLa
TumCMig↓, DNMTs↓, HDAC↓, HATs↓, ac‑H3↓, ac‑H4↓, MMP2↓, MMP9↓, HO-1↓, E-cadherin↑, EZH2↓, HER2/EBBR2↓, IL18↓, IL8↓, IL2↓,
1100- LT,    Luteolin, a flavonoid, as an anticancer agent: A review
- Review, NA, NA
TumCP↓, TumCCA↑, Apoptosis↑, EMT↓, E-cadherin↑, N-cadherin↓, Snail↓, Vim↓, ROS↑, ER Stress↑, mtDam↑, p‑eIF2α↝, p‑PERK↝, p‑CHOP↝, p‑ATF4↝, cl‑Casp12↝,
2905- LT,    Luteolin blocks the ROS/PI3K/AKT pathway to inhibit mesothelial-mesenchymal transition and reduce abdominal adhesions
- in-vivo, NA, HMrSV5
*ROS↓, *p‑Akt↓, *Vim↓, *E-cadherin↑, *PI3K↓,

Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

Catalase↓, 1,   HO-1↓, 2,   NRF2↓, 2,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 4,   SOD↓, 2,   Trx1↑, 1,  

Metal & Cofactor Biology

IronCh↑, 1,  

Mitochondria & Bioenergetics

BOK↑, 1,   CDC2↓, 2,   MMP↓, 2,   mtDam↑, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis

AKT1↓, 1,   cMyc↓, 1,   p‑cMyc↑, 1,  

Cell Death

Akt↓, 2,   Akt↑, 1,   p‑Akt↓, 1,   APAF1↑, 1,   Apoptosis↑, 2,   BAD↑, 1,   BAX↑, 3,   Bcl-2↓, 2,   BID↑, 1,   cl‑Casp12↑, 1,   cl‑Casp12↝, 1,   Casp3↑, 2,   cl‑Casp3↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 2,   cl‑Casp9↑, 1,   proCasp9↓, 1,   Cyt‑c↑, 2,   DR5↑, 3,   FADD↑, 1,   Fas↑, 1,   hTERT/TERT↓, 3,   iNOS↓, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   MDM2↓, 2,   NAIP↓, 1,   NICD↓, 1,   survivin↓, 1,   Telomerase↓, 2,   YAP/TEAD↓, 1,  

Kinase & Signal Transduction

HER2/EBBR2↓, 1,  

Transcription & Epigenetics

EZH2↓, 1,   ac‑H3↓, 1,   ac‑H4↓, 1,   HATs↓, 1,  

Protein Folding & ER Stress

p‑CHOP↝, 1,   eIF2α↑, 1,   p‑eIF2α↝, 1,   ER Stress↑, 3,   PERK↑, 1,   p‑PERK↝, 1,  

Autophagy & Lysosomes

Beclin-1↑, 2,   BNIP3↑, 1,   LC3B-II↑, 1,   LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair

DNAdam↑, 1,   DNMTs↓, 1,   P53↑, 2,   cl‑PARP↑, 1,  

Cell Cycle & Senescence

CDK2↓, 4,   CDK4↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State

EMT↓, 4,   ERK↓, 1,   p‑ERK↓, 1,   p‑GSK‐3β↓, 1,   HDAC↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   PI3K↓, 3,   RAS↓, 1,   p‑STAT3↓, 1,   TAZ↓, 1,   Wnt↓, 1,  

Migration

AEG1↓, 1,   Akt2↓, 1,   Ca+2↑, 2,   E-cadherin↑, 5,   FAK↓, 1,   MMP2↓, 3,   MMP9↓, 3,   N-cadherin↓, 4,   Snail↓, 2,   TIMP1↑, 1,   TIMP2↑, 1,   TumCMig↓, 1,   TumCP↓, 3,   Twist↓, 1,   Vim↓, 3,  

Angiogenesis & Vasculature

angioG↓, 2,   ATF4↑, 1,   p‑ATF4↝, 1,   p‑EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 2,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling

COX2↓, 1,   CXCR4↓, 1,   IFN-γ↓, 1,   IL1↓, 1,   IL18↓, 1,   IL2↓, 1,   IL6↓, 1,   IL8↓, 1,   NF-kB↓, 3,   p‑NF-kB↑, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors

AR↓, 1,  

Drug Metabolism & Resistance

ChemoSen↓, 1,   ChemoSen↑, 2,   MDR1↓, 1,   RadioS↑, 1,  

Clinical Biomarkers

AR↓, 1,   p‑EGFR↓, 1,   EZH2↓, 1,   GutMicro↑, 1,   HER2/EBBR2↓, 1,   hTERT/TERT↓, 3,   IL6↓, 1,  

Functional Outcomes

cardioP↑, 1,  
Total Targets: 135

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 2,   Catalase↑, 1,   GSH↑, 1,   GSR↑, 1,   GSTs↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 3,   SOD↑, 2,  

Metal & Cofactor Biology

IronCh↑, 1,  

Mitochondria & Bioenergetics

MMP↑, 1,  

Core Metabolism/Glycolysis

LDHA↑, 1,  

Cell Death

p‑Akt↓, 1,  

Autophagy & Lysosomes

Beclin-1↓, 1,  

Proliferation, Differentiation & Cell State

PI3K↓, 1,  

Migration

E-cadherin↑, 1,   Vim↓, 1,  

Angiogenesis & Vasculature

NO↓, 1,  

Barriers & Transport

BBB↑, 1,  

Synaptic & Neurotransmission

AChE↓, 1,  

Protein Aggregation

Aβ↓, 1,  

Drug Metabolism & Resistance

BioAv↓, 3,   BioAv↑, 1,  

Functional Outcomes

neuroP↑, 2,   toxicity↓, 1,  
Total Targets: 25

Scientific Paper Hit Count for: E-cadherin, E-cadherin
6 Luteolin
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#:118  Target#:89  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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