Luteolin / cMET 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

cMET, cellular hepatocyte growth factor receptor: Click to Expand ⟱

Source:

Type:

c-MET, also known as the hepatocyte growth factor receptor (HGFR), is a receptor tyrosine kinase that plays a crucial role in various cellular processes, including cell proliferation, survival, migration, and differentiation. It is activated by its ligand, hepatocyte growth factor (HGF). Dysregulation of the c-MET signaling pathway has been implicated in several types of cancer.

c-Met is often overexpressed or mutated in cancer and is associated with poor prognosis, increased metastasis, and resistance to therapies.

Scientific Papers found: Click to Expand⟱

1200-

LT,

Inhibition of Fatty Acid Synthase by Luteolin Post-Transcriptionally Downregulates c-Met Expression Independent of Proteosomal/Lysosomal Degradation

in-vitro,

Pca,

DU145

luteolin could act as a novel HGF/c-Met inhibitor

FASN↓, cMET↓, HGF/c-Met↓,

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:

Core Metabolism/Glycolysis ⓘ

FASN↓, 1,

Cell Death ⓘ

HGF/c-Met↓, 1,

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 1,
Total Targets: 3

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: cMET, cellular hepatocyte growth factor receptor

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