Urolithin / MCP1 Cancer Research Results

Uro, Urolithin: Click to Expand ⟱
Features:
Urolithins are gut microbiota–derived dibenzopyran-6-one metabolites formed from ellagitannins → ellagic acid. They are the bioactive, systemically relevant forms responsible for most of the anticancer, mitochondrial, and signaling effects attributed to pomegranate and berry consumption.
Ellagic acid itself is largely confined to the gut lumen; urolithins are what reach circulation and tissues.

Urolithin A (UA), Most studied; mitophagy, anticancer, anti-inflammatory
Humans fall into urolithin metabotypes:
Metabotype	Description	            Approx. Population
A	        Produces UA (best profile)	~40%
B	        Produces UB ± UA	       ~25–30%
0	        Non-producer	                ~30%

ROS Modulation (Context-Dependent)
Cancer cells:
-Mild ROS ↑ or redox stress → apoptosis, growth arrest
Normal cells:
-ROS ↓, improved mitochondrial efficiency

This duality is why urolithins are less chemo-antagonistic than classic antioxidants.

Anticancer Signaling
↓ PI3K/AKT/mTOR
↓ Wnt/β-catenin
↓ NF-κB, STAT3
Cell-cycle arrest (G1/S)

Unlike sulforaphane or NAC, urolithins:
-Do not strongly upregulate NRF2 in cancer cells
-May normalize NRF2 signaling in normal cells
Direct Urolithin A Supplements: Bypass microbiome dependency

Urolithin A–type activity — Cancer vs Normal Cell Effects
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Mitophagy / mitochondrial quality control (PINK1–Parkin axis) ↑ mitophagy → loss of mitochondrial reserve ↑ mitophagy → improved mitochondrial fitness Driver Mitochondrial pruning and quality enforcement Urolithins selectively stress cancer cells by removing dysfunctional mitochondria while rejuvenating normal-cell mitochondrial pools
2 Mitochondrial metabolism / bioenergetics ↓ metabolic flexibility; ↓ ATP resilience ↑ oxidative efficiency Driver Energy stress vs optimization Cancer cells are less able to compensate for enforced mitochondrial turnover
3 Reactive oxygen species (ROS) ↑ ROS (secondary to mitochondrial stress) ↓ ROS Secondary Metabolism-linked redox shift ROS changes arise from altered mitochondrial populations, not direct redox cycling
4 AMPK / mTOR nutrient-sensing axis ↑ AMPK; ↓ mTOR signaling ↑ AMPK (adaptive) Secondary Catabolic pressure and growth restraint Energy-sensing pathways reinforce growth suppression in metabolically stressed tumor cells
5 Cell cycle regulation ↓ proliferation / ↑ arrest ↔ spared Phenotypic Cytostatic growth limitation Growth inhibition reflects bioenergetic insufficiency rather than direct CDK inhibition
6 Inflammatory signaling (NF-κB / cytokines) ↓ pro-tumor inflammation ↓ inflammatory tone Secondary Anti-inflammatory modulation Reduced inflammation contributes to chemopreventive and microenvironmental effects
7 NRF2 antioxidant response ↑ NRF2 (adaptive, secondary) ↑ NRF2 (protective) Adaptive Redox homeostasis reinforcement NRF2 activation reflects improved mitochondrial quality and reduced oxidative burden rather than a cytotoxic mechanism
8 Apoptosis sensitivity ↑ sensitivity to apoptosis (stress-context dependent) ↓ apoptosis Phenotypic Threshold-dependent cell death Apoptosis occurs when mitochondrial and energetic stress exceed adaptive capacity


MCP1, CCL2,monocyte chemotactic protein-1: Click to Expand ⟱
Source:
Type:
MCP-1 (Monocyte Chemoattractant Protein-1, also known as CCL2)
MCP-1/CCL2 is a chemokine involved in recruiting monocytes, memory T cells, and dendritic cells to sites of inflammation.
– It plays a key role in mediating immune cell trafficking, inflammation, and tissue remodeling. MCP-1 is pivotal in inflammatory responses and can modulate immune cell infiltration into tissues.
– It also influences the polarization of macrophages, which may adopt pro-inflammatory (M1) or anti-inflammatory/pro-tumoral (M2) roles.

Many cancers (such as breast, prostate, ovarian, lung, and colon cancers) exhibit increased levels of MCP-1.
– Both tumor cells and associated stromal cells (e.g., cancer-associated fibroblasts, infiltrating immune cells) can produce MCP-1, contributing to an inflammatory milieu.

• Inducers of MCP-1:
– Hypoxia, oncogenic pathways, and cytokine-rich environments (e.g., IL-1β, TNF-α) can drive increased MCP-1 expression.
– This upregulation often correlates with an ongoing inflammatory response in the tumor microenvironment.
Scientific Papers found: Click to Expand⟱
4861- Uro,    Urolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions
- in-vivo, AD, NA
*memory↑, *Aβ↓, *toxicity↓, *BBB↑, *p‑tau↓, *eff↓, *IL1α↓, *MCP1↓, *MIP‑1α↓, *TNF-α↓, *IL2↓, *SIRT1↓, *DNAdam↓, *Dose↝, *Strength↑, *motorD↑, *CTSZ↓,

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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

SIRT1↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

CTSZ↓, 1,   IL1α↓, 1,   IL2↓, 1,   MCP1↓, 1,   MIP‑1α↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

p‑tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   eff↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   motorD↑, 1,   Strength↑, 1,   toxicity↓, 1,  
Total Targets: 17

Scientific Paper Hit Count for: MCP1, CCL2,monocyte chemotactic protein-1
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#:383  Target#:990  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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