Rutin / N-cadherin Cancer Research Results

RT, Rutin: Click to Expand ⟱
Features:
Rutin, a Quercetin Glycoside
Rutin, a natural flavonoid glycoside found in many plants like buckwheat, citrus fruits, and apples, has shown promising neuroprotective and anticancer properties.
Rutin is a flavonoid glycoside composed of quercetin bound to the disaccharide rutinose. It is widely found in buckwheat, citrus fruits, apples, and tea. In cancer models, rutin exhibits antioxidant, anti-inflammatory, anti-proliferative, and pro-apoptotic effects. Because it is glycosylated, rutin itself has relatively low cellular permeability; many biological effects are mediated after intestinal hydrolysis to quercetin and subsequent phase-II metabolites. Mechanistically, rutin is most consistently associated with suppression of NF-κB and PI3K/AKT signaling, modulation of MAPK pathways, redox regulation (Nrf2/ROS balance), inhibition of angiogenesis (VEGF), and induction of cell-cycle arrest and apoptosis in preclinical systems. Effects are model-dependent and often concentration-dependent, with antioxidant behavior dominating in normal tissue contexts and context-dependent pro-oxidant effects described in some tumor settings.
-Scavenges free radicals, reduces oxidative stress
-Inhibits pro-inflammatory cytokines like IL-1β, TNF-α, and reduces activation of NF-κB.
-Inhibition of Aβ Aggregation (AD)
-Mild inhibitory effects on acetylcholinesterase (AChE), helping enhance cholinergic function.
-May upregulate BDNF expression

Cancer:
-Induces cell cycle arrest in G2/M phase.
-Inhibits VEGF, Suppresses MMP-2 and MMP-9
-Inhibits PI3K/Akt/mTOR, MAPK, and NF-κB signaling pathways.
-Enhances sensitivity to Chemotherapy drugs like doxorubicin and cisplatin

Rutin has poor oral bioavailability, but this can be improved with nanoformulations or co-administration with absorption enhancers like piperine or quercetin.


Cancer Pathway Table: Rutin

Rank Pathway / Axis Cancer / Tumor Context Normal Tissue Context TSF Primary Effect Notes / Interpretation
1 NF-κB inflammatory / survival signaling NF-κB ↓; COX-2, cytokines ↓ (reported) Inflammatory tone ↓ R, G Anti-inflammatory / anti-survival Frequently reported mechanism; contributes to reduced tumor-promoting inflammation and survival signaling.
2 PI3K → AKT → mTOR axis PI3K/AKT ↓; proliferation ↓ (model-dependent) ↔ R, G Growth signaling suppression Observed in several tumor models; often secondary to upstream redox and inflammatory modulation.
3 Cell-cycle regulation (Cyclins/CDKs; G1 or G2/M arrest) Cell-cycle arrest ↑ (reported) ↔ G Cytostasis Associated with reduced Cyclin D1/CDK expression; typically downstream of survival pathway inhibition.
4 Intrinsic apoptosis (mitochondrial pathway) Bax ↑; Bcl-2 ↓; caspases ↑ (reported) Minimal activation at lower exposure G Apoptotic execution Apoptosis induction frequently reported in vitro; magnitude depends on achievable intracellular concentration.
5 ROS modulation (biphasic redox behavior) ROS ↑ in some tumor contexts; apoptosis ↑ ROS ↓ (antioxidant protection) P, R Redox modulation Rutin is classically antioxidant but may promote oxidative stress in tumor cells under certain conditions (dose/metal-dependent).
6 Nrf2 / ARE antioxidant response Context-dependent modulation Nrf2 ↑; antioxidant enzymes ↑ R, G Redox buffering Common polyphenol signature; may protect normal tissue from oxidative injury.
7 MAPK pathways (ERK / JNK / p38) Stress-MAPK modulation (context-dependent) ↔ P, R, G Signal reprogramming JNK/p38 activation reported in apoptosis contexts; ERK modulation varies by model.
8 Angiogenesis signaling (VEGF) VEGF ↓; angiogenic outputs ↓ (reported) ↔ G Anti-angiogenic support Often secondary to NF-κB and PI3K suppression.
9 Invasion / metastasis (MMPs / EMT) MMP2/MMP9 ↓; migration ↓ (reported) ↔ G Anti-invasive phenotype Typically downstream of inflammatory and MAPK modulation.
10 Bioavailability constraint (glycoside → quercetin metabolism) Systemic exposure mainly as metabolites — — Translation constraint Rutin has limited direct cellular uptake; many effects likely mediated after conversion to quercetin and phase-II metabolites.

TSF: P = 0–30 min (rapid redox interactions), R = 30 min–3 hr (acute signaling shifts), G = >3 hr (gene-regulatory adaptation and phenotype outcomes).



Alzheimer’s Disease (AD) Summary — Rutin

Rutin has been studied in preclinical neurodegeneration models for its antioxidant, anti-inflammatory, and mitochondrial-protective properties. It is reported to modulate Nrf2 signaling, suppress NF-κB–mediated neuroinflammation, reduce oxidative stress, and attenuate amyloid-β–induced neuronal injury in experimental systems. Many effects may be mediated after hydrolysis to quercetin. Human clinical evidence remains limited.


Alzheimer’s Disease Table: Rutin

Rank Pathway / Axis AD / Neurodegeneration Context Normal Brain Context TSF Primary Effect Notes / Interpretation
1 Nrf2 / ARE antioxidant response Nrf2 ↑; HO-1 ↑; GSH ↑; oxidative damage ↓ (reported) Redox homeostasis support R, G Antioxidant neuroprotection Consistent polyphenol signature; reduces lipid peroxidation and ROS markers in AD models.
2 NF-κB / neuroinflammation Microglial activation ↓; TNF-α / IL-1β ↓ (reported) Inflammatory tone moderation R, G Anti-inflammatory modulation Neuroinflammation is a core AD driver; rutin shows suppression in animal models.
3 Amyloid-β toxicity modulation Aβ-induced ROS ↓; neuronal apoptosis ↓ (reported) ↔ G Anti-amyloid support Evidence mainly from in vitro and rodent models; not confirmed clinically.
4 Mitochondrial protection ΔΨm stabilization; ATP preservation (reported) Mitochondrial resilience R Bioenergetic protection Opposes mitochondrial dysfunction induced by oxidative stress.
5 MAPK (JNK / p38 stress signaling) Stress-MAPK suppression (reported) ↔ P, R Stress signaling reduction JNK/p38 activation linked to neuronal apoptosis; suppression reported in models.
6 Cholinergic signaling (reported in some models) AChE activity ↓ (reported) ↔ G Cognitive support (model-based) Evidence limited; magnitude smaller than pharmaceutical AChE inhibitors.
7 BBB penetration (metabolite-driven) Effects likely via quercetin metabolites Systemic metabolism required — Translation constraint Parent rutin has limited direct brain penetration; hydrolysis/metabolism important.
8 Clinical evidence Limited human AD trials — — Evidence constraint Most data preclinical; not established as AD therapy.

TSF: P = 0–30 min (early signaling modulation), R = 30 min–3 hr (stress-response shifts), G = >3 hr (gene-regulatory and neuroprotective outcomes).



N-cadherin, N-cadherin: Click to Expand ⟱
Source:
Type:
Also known as Cadherin2 (CDH2).
N-cadherin is a type of cell adhesion molecule that plays a crucial role in the development and maintenance of tissue structure. In the context of cancer, N-cadherin has been implicated in the progression and metastasis of various types of tumors.
N-cadherin expression is increased in various types of cancer.
Normally, N-cadherin is expressed in mesenchymal cells, such as fibroblasts and smooth muscle cells. However, in cancer cells, N-cadherin expression is often upregulated, which can contribute to the epithelial-to-mesenchymal transition (EMT). EMT is a process by which epithelial cells acquire a more mesenchymal phenotype, which is characterized by increased motility, invasiveness, and resistance to apoptosis.
The expression of N-cadherin in cancer cells is closely associated with tumorigenesis and metastasis. Additionally, the soluble N-cadherin level in the serum of cancer patients is much higher than that in the serum of healthy patients, revealing a positive relation with poor prognosis.
Scientific Papers found: Click to Expand⟱
1132- RT,    Rutin Promotes Proliferation and Orchestrates Epithelial–Mesenchymal Transition and Angiogenesis in MCF-7 and MDA-MB-231 Breast Cancer Cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
Vim↑, N-cadherin↑, E-cadherin↓, TumCP↑, TumCMig↑, tumCV↑, MKI67↑,

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:


Transcription & Epigenetics ⓘ

tumCV↑, 1,  

Migration ⓘ

E-cadherin↓, 1,   N-cadherin↑, 1,   TumCMig↑, 1,   TumCP↑, 1,   Vim↑, 1,  

Functional Outcomes ⓘ

MKI67↑, 1,  
Total Targets: 7

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: N-cadherin, N-cadherin
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#:143  Target#:355  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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