Myricetin / F-actin Cancer Research Results

Myr, Myricetin: Click to Expand ⟱
Features:
Myricetin (MYR; 3,3′,4′,5,5′,7-hexahydroxyflavone) is a dietary flavonol polyphenol abundant in berries, tea, red wine, and some medicinal plants. Its dominant biology is redox-active modulation with context-dependent pro-oxidant capacity, ranking conceptually as:
(1) ROS modulation (scavenging at low dose; pro-oxidant at higher dose or with metal redox cycling),
(2) PI3K/Akt/mTOR and MAPK pathway inhibition,
(3) NF-κB suppression and inflammatory signaling control, and
(4) mitochondrial apoptosis induction (caspase activation, ΔΨm disruption).
Bioavailability is limited by low aqueous solubility and rapid conjugation (glucuronidation/sulfation); reported human plasma levels after dietary exposure are typically sub-micromolar (<1 µM), while many in-vitro cancer studies use 10–100 µM, often exceeding realistic systemic exposure. Clinical evidence remains preclinical-dominant; no robust RCT-grade anticancer efficacy established. Redox duality implies potential chemo-sensitization in oxidative tumors but also theoretical protection of normal tissue.

-Possible inhibitory effects on mammalian TrxRs (thioredoxin reductase)

Myricetin (MYR) — Cancer-Relevant Pathway Effects

Rank Pathway / Axis Cancer Cells (↑/↓/↔ + qualifiers) Normal Cells (↑/↓/↔ + qualifiers) TSF Primary Effect Notes / Interpretation
1 ROS Modulation ↑ ROS (high conc., pro-oxidant); ↓ ROS (low conc.) ↓ ROS (protective; dose-dependent) P–R Redox stress induction or buffering Metal-chelating flavonol; can shift to pro-oxidant under tumor oxidative stress, enabling apoptosis.
2 PI3K/Akt/mTOR ↓ Akt phosphorylation (model-dependent) ↔ / mild inhibition R–G Anti-proliferative signaling Common in breast, colon, and prostate cell models; often ≥10 µM required.
3 MAPK (ERK/JNK/p38) ↓ ERK; ↑ JNK/p38 (stress-activated; context) ↔ / adaptive stress response R Pro-apoptotic signaling shift Promotes apoptotic cascades via stress kinase activation.
4 NF-κB ↓ NF-κB activation ↓ NF-κB (anti-inflammatory) R–G Anti-inflammatory modulation May reduce tumor-promoting inflammation.
5 Mitochondrial Apoptosis (Caspase / ΔΨm) ↑ Bax; ↓ Bcl-2; ↑ caspase-3 ↔ / protective at low dose R–G Intrinsic apoptosis activation Frequently observed in leukemia and solid tumor models at supra-physiologic doses.
6 NRF2 Axis ↔ / mild ↑ (context-dependent) ↑ NRF2 (cytoprotection) R–G Adaptive antioxidant response Less potent NRF2 activator than electrophilic isothiocyanates.
7 Ca²⁺ Signaling ↑ intracellular Ca²⁺ (mitochondrial stress; model-dependent) ↔ R Apoptosis facilitation Reported in some hepatoma and leukemia models.
8 Ferroptosis ↔ / potentially ↓ (iron-chelating) ↔ — Lipid peroxidation modulation Chelation may counter ferroptosis unless combined with pro-oxidant triggers.
9 Clinical Translation Constraint Low oral bioavailability; plasma <1 µM; most anticancer studies use 10–100 µM — PK limitation Conjugation and rapid metabolism limit systemic tumor exposure.
TSF Legend: P: 0–30 min   R: 30 min–3 hr   G: >3 hr
F-actin, fibrous actin: Click to Expand ⟱
Source:
Type:
A fibrous actin polymerized in the form of a double helix that is produced in the presence of a metal cation (as of calcium) and ATP.
Dynamic rearrangements of the F-actin cytoskeleton are a hallmark of tumor metastasis.

F-actin plays a significant role in the progression and prognosis of various cancers. Its expression and dynamics are often linked to increased invasiveness, metastatic potential, and treatment resistance. In many cancer types, high levels of F-actin correlate with poor prognosis and aggressive disease.


Scientific Papers found: Click to Expand⟱
1141- Myr,    Myricetin: targeting signaling networks in cancer and its implication in chemotherapy
- Review, NA, NA
*PI3K↑, *Akt↑, p‑Akt↓, SIRT3↑, p‑ERK↓, p38↓, VEGF↓, MEK↓, MKK4↓, MMP9↓, Raf↓, F-actin↓, MMP2↓, COX2↓, BMP2↓, cycD1/CCND1↓, Bax:Bcl2↑, EMT↓, EGFR↓, TumAuto↑,

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 ⓘ

SIRT3↑, 1,  

Mitochondria & Bioenergetics ⓘ

MEK↓, 1,   MKK4↓, 1,   Raf↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Bax:Bcl2↑, 1,   BMP2↓, 1,   p38↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   p‑ERK↓, 1,  

Migration ⓘ

F-actin↓, 1,   MMP2↓, 1,   MMP9↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Akt↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↑, 1,  
Total Targets: 2

Scientific Paper Hit Count for: F-actin, fibrous actin
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#:127  Target#:565  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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