Luteolin / Vim 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


Vim, Vimentin: Click to Expand ⟱
Source:
Type:
Vimentin, a major constituent of the intermediate filament family of proteins, is ubiquitously expressed in normal mesenchymal cells and is known to maintain cellular integrity and provide resistance against stress. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.

In many epithelial-derived tumors (carcinomas), elevated Vimentin expression is often observed in cancer cells that have undergone EMT. This upregulation is characteristic of a shift toward a mesenchymal state, which is associated with reduced cell–cell adhesion and increased motility. Vimentin expression is also noted in the tumor stroma, reflecting the presence and activation of mesenchymal cells such as cancer-associated fibroblasts (CAFs). This dual expression can contribute to the remodeling of the tumor microenvironment.
The degree of Vimentin expression may vary depending on the tumor type, grade, and stage. More aggressive and advanced tumors tend to show higher levels of Vimentin expression.

High Vimentin expression has been correlated with poor clinical outcomes in several cancers, including breast, colorectal, prostate, and lung cancers.
Elevated Vimentin levels are typically associated with higher tumor grade, increased invasiveness, enhanced metastatic potential, and a greater risk of recurrence.
As a component of the EMT signature, high Vimentin expression can serve as an indicator of a more aggressive tumor phenotype and is often associated with reduced overall survival.
- vimentin up-regulation is often used as a marker of EMT in cancer



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↑,
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↑,
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 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 ⓘ

Catalase↓, 1,   NRF2↓, 1,   ROS↓, 1,   ROS↑, 3,   SOD↓, 2,   Trx1↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

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

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   cMyc↓, 1,  

Cell Death ⓘ

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

Protein Folding & ER Stress ⓘ

p‑CHOP↝, 1,   eIF2α↑, 1,   p‑eIF2α↝, 1,   ER Stress↑, 2,   PERK↑, 1,   p‑PERK↝, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 2,   BNIP3↑, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 3,   CDK4↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 3,   p‑ERK↓, 1,   NOTCH↓, 1,   PI3K↓, 2,   p‑STAT3↓, 1,  

Migration ⓘ

Akt2↓, 1,   Ca+2↑, 1,   E-cadherin↑, 3,   FAK↓, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 3,   Snail↓, 2,   TumCP↓, 2,   Twist↓, 1,   Vim↓, 3,  

Angiogenesis & Vasculature ⓘ

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

Immune & Inflammatory Signaling ⓘ

IL1↓, 1,   IL6↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Clinical Biomarkers ⓘ

p‑EGFR↓, 1,   GutMicro↑, 1,   hTERT/TERT↓, 2,   IL6↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,  
Total Targets: 86

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

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

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↓, 2,  

Functional Outcomes ⓘ

neuroP↑, 2,  
Total Targets: 22

Scientific Paper Hit Count for: Vim, Vimentin
4 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#:336  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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