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| 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 cellsDirect Urolithin A Supplements: Bypass microbiome dependency Urolithin A–type activity — Cancer vs Normal Cell Effects
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| Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms: 1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion. 2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue. 3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment. 4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream. 5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body. 6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection. 7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs. 8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis. |
| 4844- | Uro, | Urolithin A Inhibits Epithelial–Mesenchymal Transition in Lung Cancer Cells via P53-Mdm2-Snail Pathway |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Lung, | H460 |
| 4849- | Uro, | Urolithin A suppresses tumor progression and induces autophagy in gastric cancer via the PI3K/Akt/mTOR pathway |
| - | vitro+vivo, | GC, | NA |
| 4851- | Uro, | Urolithin A suppressed osteosarcoma cell migration and invasion via targeting MMPs and AKT1 |
| - | in-vitro, | OS, | MG63 |
| 4856- | Uro, | Study on the biological mechanism of urolithin a on nasopharyngeal carcinoma in vitro |
| - | in-vitro, | NPC, | CNE1 | - | in-vitro, | NPC, | CNE2 |
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
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