Urolithin / TumCCA 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


TumCCA, Tumor cell cycle arrest: Click to Expand ⟱
Source:
Type:
Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases. S, G1, G2, and M are the four phases of mitosis.
Scientific Papers found: Click to Expand⟱
4857- Uro,    Evaluation and comparison of the anti-proliferative and anti-metastatic effects of urolithin A and urolithin B against esophageal cancer cells: an in vitro and in silico study
- in-vitro, ESCC, KYSE-30
tumCV↓, selectivity↑, TumCCA↑, ROS↑, Bcl-2↓, BAX↑, P21↑, MMP2↓, MMP9↓,
4845- Uro,    The gut microbiota metabolite urolithin A, but not other relevant urolithins, induces p53-dependent cellular senescence in human colon cancer cells
- in-vitro, Colon, HCT116
TumCCA↑, P53↑, P21↑,
4835- Uro,    Urolithin A, induces apoptosis and autophagy crosstalk in Oral Squamous Cell Carcinoma via mTOR /AKT/ERK1/2 pathway
- in-vitro, SCC, NA
TumCD↑, ER Stress↑, Akt↓, mtDam↓, p‑mTOR↓, *BioAv↝, ROS↑, TumCCA↑, Apoptosis↑, ERK↓,
4837- Uro,    Urolithins: The Gut Based Polyphenol Metabolites of Ellagitannins in Cancer Prevention, a Review
- Review, Var, NA
AntiCan↑, TumCCA↑, Apoptosis↑, TumAuto↑, *BioAv↝, *BioAv↑, RAS↓, ERK↓, AR↓, TumCP↓, PI3K↓, Akt↓, NF-kB↓, COX2↓, IL6↓, IL1β↓, Wnt↓, β-catenin/ZEB1↓, cMyc↓, P53↑, Casp3↑, PARP↑, ROS↓, toxicity↓,
4841- Uro,    Urolithin A induces cell cycle arrest and apoptosis by inhibiting Bcl-2, increasing p53-p21 proteins and reactive oxygen species production in colorectal cancer cells
- in-vitro, CRC, HT29 - in-vitro, CRC, SW480 - in-vitro, CRC, SW-620
TumCP↓, TumCCA↑, Apoptosis↑, P53↑, P21↑, Bcl-2↓, Cyt‑c↑, Casp↑, ROS↑, *ROS↓,
4833- Uro,    Unveiling the potential of Urolithin A in Cancer Therapy: Mechanistic Insights to Future Perspectives of Nanomedicine
- Review, Var, NA - Review, AD, NA - Review, IBD, NA
BioAv↝, TumAuto↝, TumCG↓, TumMeta↓, ChemoSen↑, Imm↑, RadioS↑, BioAv↑, other↝, eff↓, *antiOx↓, *Inflam↓, AntiCan↓, AntiAge↑, chemoP↑, *neuroP↑, *ROS↓, *cognitive↑, *lipid-P↓, *cardioP↑, *TNF-α↓, *IL6↓, GutMicro↑, TumCCA↑, Apoptosis↑, angioG↓, NF-kB↓, PI3K↓, Akt↓, Casp↑, survivin↓, TumCP↓, cycD1/CCND1↓, cMyc↑, BAX↑, Bcl-2↓, COX2↓, P53↑, p38↑, *ROS↓, *SOD↑, *GPx↑, SIRT1↑, FOXO1↑, eff↑, ChemoSen↑,
4847- Uro,    Metabolite of ellagitannins, urolithin A induces autophagy and inhibits metastasis in human sw620 colorectal cancer cells
- in-vitro, CRC, SW-620
TumCP↓, TumCMig↓, MMP9↓, TumAuto↑, Apoptosis↑, TumCCA↓, TumMeta↓, ChemoSen↓,
4852- Uro,    Dietary Urolithin B Suppresses Lung Tumorigenesis Correlating with Autophagy Induction and Gut Microbiota Remodeling
- vitro+vivo, Lung, NA
TumCG↓, *GutMicro↑, *Inflam↓, *antiOx↑, AntiTum↑, TumCCA↑, Apoptosis↑,
4855- Uro,    Urolithins impair cell proliferation, arrest the cell cycle and induce apoptosis in UMUC3 bladder cancer cells
- in-vitro, Bladder, UMUC3
TumCCA↑, PI3K↓, Akt↓, MAPK↓,

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   cMyc↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 4,   Apoptosis↑, 6,   BAX↑, 2,   Bcl-2↓, 3,   Casp↑, 2,   Casp3↑, 1,   Cyt‑c↑, 1,   MAPK↓, 1,   p38↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,   TumAuto↝, 1,  

DNA Damage & Repair ⓘ

P53↑, 4,   PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 3,   TumCCA↓, 1,   TumCCA↑, 8,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 2,   FOXO1↑, 1,   p‑mTOR↓, 1,   PI3K↓, 3,   RAS↓, 1,   TumCG↓, 2,   Wnt↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 2,   TumCMig↓, 1,   TumCP↓, 4,   TumMeta↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL1β↓, 1,   IL6↓, 1,   Imm↑, 1,   NF-kB↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,   ChemoSen↓, 1,   ChemoSen↑, 2,   eff↓, 1,   eff↑, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↓, 1,   AntiCan↑, 1,   AntiTum↑, 1,   chemoP↑, 1,   toxicity↓, 1,  
Total Targets: 65

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 1,   GPx↑, 1,   lipid-P↓, 1,   ROS↓, 3,   SOD↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   Inflam↓, 2,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 2,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 1,   neuroP↑, 1,  
Total Targets: 16

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest
9 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#:322  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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