Urolithin / Catalase 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


Catalase, Catalase: Click to Expand ⟱
Source:
Type:
Caspases are a cysteine protease that speed up a chemical reaction via pointing their target substrates following an aspartic acid residue.1 They are grouped into apoptotic (caspase-2, 3, 6, 7, 8, 9 and 10) and inflammatory (caspase-1, 4, 5, 11 and 12) mediated caspases.
Caspase-1 may have both tumorigenic or antitumorigenic effects on cancer development and progression, but it depends on the type of inflammasome, methodology, and cancer.
Catalase is an enzyme found in nearly all living cells exposed to oxygen. Its primary role is to protect cells from oxidative damage by catalyzing the conversion of hydrogen peroxide (H₂O₂), a potentially damaging byproduct of metabolism, into water (H₂O) and oxygen (O₂). This detoxification process is crucial because excess H₂O₂ can lead to the formation of reactive oxygen species (ROS) that damage proteins, lipids, and DNA.

Catalase and Cancer
Oxidative Stress and Cancer:
Cancer cells often experience increased levels of oxidative stress due to rapid proliferation and metabolic changes. This stress can lead to DNA damage, promoting tumorigenesis.
Catalase helps mitigate oxidative stress, and its expression can influence the survival and proliferation of cancer cells.
Expression Levels in Different Cancers:
Overexpression: In some cancers, such as breast cancer and certain types of leukemia, catalase may be overexpressed. This overexpression can help cancer cells survive in oxidative environments, potentially leading to more aggressive tumor behavior.
Downregulation: Conversely, in other cancers, such as colorectal cancer, reduced catalase expression has been observed. This downregulation can lead to increased oxidative stress, contributing to tumor progression and metastasis.
Prognostic Implications:
Survival Rates: Studies have shown that high levels of catalase expression can be associated with poor prognosis in certain cancers, as it may enable cancer cells to resist apoptosis (programmed cell death) induced by oxidative stress.

Some types of cancer cells have been reported to exhibit lower catalase activity, possibly increasing their vulnerability to oxidative damage under certain conditions. This vulnerability has even been exploited in some therapeutic strategies (for example, approaches that generate excess H₂O₂ or other ROS specifically targeting cancer cells have been researched).
Scientific Papers found: Click to Expand⟱
4858- Uro,    The Metabolite Urolithin-A Ameliorates Oxidative Stress in Neuro-2a Cells, Becoming a Potential Neuroprotective Agent
- in-vitro, Nor, NA
*ROS?, *neuroP↑, *lipid-P↓, *Catalase↑, *SOD↑, *GPx↑, *GSR↑, *monoA↓, *tyrosinase↓,
4869- Uro,    Urolithin A in Central Nervous System Disorders: Therapeutic Applications and Challenges
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*MitoP↑, *Inflam↓, *antiOx↑, *Risk↓, *Aβ↓, *p‑tau↓, *p62↓, *PARK2↑, *MMP↑, *ROS↓, *Strength↑, *CRP↓, *IL1β↓, *IL6↓, *TNF-α↓, *AMPK↑, *NF-kB↓, *MAPK↓, *p62↑, *NRF2↑, *SOD↑, *Catalase↑, *HO-1↑, *Ferroptosis↓, *lipid-P↓, *Cartilage↑, *PI3K↓, *Akt↓, *mTOR↓, *Apoptosis↓, *neuroP↑, *Bcl-2↓, *BAX↑, *Casp3↑, *ATP↑, *eff↑, *motorD↑, *NLRP3↓, *radioP↑, *BBB↑,
4876- Uro,    Urolithin A in Health and Diseases: Prospects for Parkinson’s Disease Management
- Review, Park, NA - Review, AD, NA
*Inflam↓, *antiOx↓, *neuroP↑, *p‑tau↓, *Aβ↓, *eff↑, *BioAv↓, *BioAv↑, *GSH↑, *SOD↑, *lipid-P↓, *Catalase↑, *GSR↑, *GPx↑, *ROS↓, *NRF2↑, *GutMicro↑, *Risk↓, *BBB↓, *NLRP3↓, *MAOA↓,
4880- Uro,    Urolithins: A Prospective Alternative against Brain Aging
- Review, AD, NA
*cognitive↑, *memory↑, *antiOx↑, *BBB↑, *ROS↓, *lipid-P↓, *Catalase↑, *SOD↑, *GSR↑, *GPx↑, *CREB↑, *BDNF↑, *neuroP↑, *Inflam↓, *MitoP↑, *Aβ↓, *tau↓, *NLRP3↓, *SIRT1↑, *SIRT3↑,

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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 2,   Catalase↑, 4,   Ferroptosis↓, 1,   GPx↑, 3,   GSH↑, 1,   GSR↑, 3,   HO-1↑, 1,   lipid-P↓, 4,   NRF2↑, 2,   PARK2↑, 1,   ROS?, 1,   ROS↓, 3,   SIRT3↑, 1,   SOD↑, 4,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   CREB↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Ferroptosis↓, 1,   MAPK↓, 1,  

Autophagy & Lysosomes ⓘ

MitoP↑, 2,   p62↓, 1,   p62↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,   PI3K↓, 1,   tyrosinase↓, 1,  

Migration ⓘ

Cartilage↑, 1,  

Barriers & Transport ⓘ

BBB↓, 1,   BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 3,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   MAOA↓, 1,   monoA↓, 1,   tau↓, 1,   p‑tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 3,   NLRP3↓, 3,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   eff↑, 2,  

Clinical Biomarkers ⓘ

CRP↓, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   memory↑, 1,   motorD↑, 1,   neuroP↑, 4,   radioP↑, 1,   Risk↓, 2,   Strength↑, 1,  
Total Targets: 62

Scientific Paper Hit Count for: Catalase, Catalase
4 Urolithin
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#:46  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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