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| Lignan found in bark of some magnolia species. Magnolol (MAG) — a bioactive biphenolic compound from Magnolia officinalis derived from the bark (roots and branches) of Magnolia species such as M. officinalis, M. obovata, and M. grandiflora The two main bioactive compounds isolated from these plants are MAG (5,5ʹ-diallyl-2,2ʹ-dihydroxybiphenyl) and Honokiol (3,5ʹ-diallyl-4,2ʹ-dihydroxybiphenyl) (Fig. 1) which are phenolic regioisomers. In the bark extracts of Magnolia plants, the composition of MAG ranges from 1 to 10%, while Honokiol comprises 1 to 5% Magnolol is a biphenolic neolignan isolated from the bark of Magnolia officinalis. It is structurally related to honokiol and is studied for anti-inflammatory, antioxidant, antimicrobial, and neuroactive effects. In preclinical oncology models, magnolol is reported to modulate NF-κB, STAT3, PI3K/AKT, MAPK, Wnt/β-catenin, and redox pathways, with downstream effects on cell-cycle arrest, apoptosis, invasion/EMT, and angiogenesis. Oral bioavailability is limited and many cytotoxic concentrations reported in vitro are in the tens of µM range, often above typical systemic levels from standard supplementation. major pathways and molecular targets involved in magnolol’s anticancer actions: -Apoptosis: ↑ Bax, ↓ Bcl-2, ↑ cytochrome c, ↑ caspase-9, ↑ caspase-3 -Arrests cell cycle at G0/G1 or G2/M phase:↓ Cyclin D1, CDK4, CDK6, Cyclin B1, CDK1 -Inhibits NF-κB activation: ↓ IκBα, COX-2, TNF-α -Inhibits PI3K, Akt, and mTOR phosphorylation -Suppresses angiogenesis: ↓ Bcl-XL, Mcl-1, VEGF, cyclin D1 -Inhibits β-catenin nuclear translocation -increase ROS production in tumor cells → triggers mitochondrial apoptosis -Magnolol activates Nrf2 in normal cells → upregulates HO-1, NQO1: Protects normal tissue from oxidative stress during chemotherapy or inflammation. Most in-vitro IC50 values fall in the 10–100 µM range, often above typical systemic exposure.
Time-Scale Flag (TSF): P / R / G
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| Slug is well known to promote tumor progression and metastasis through the epithelial-mesenchymal transition (EMT), causing loss of cell adhesion and polarity while conferring migratory and invasive properties. Slug/SNAI2: A transcription factor that belongs to the Snail family. It is best known for its role in regulating epithelial-to-mesenchymal transition (EMT). Expression: Upregulation of Slug in cancers is often associated with the induction of EMT. This causes cells to lose epithelial markers (like E-cadherin) and gain mesenchymal markers, leading to increased invasiveness. Metastatic Spread: By promoting EMT, high levels of Slug facilitate tumor cell dissemination and metastasis. Cancer Stem Cells: There is evidence suggesting that EMT, spurred by factors like Slug, can increase the proportion of cancer stem cells (CSCs). These CSCs are thought to be key players in tumor recurrence and maintenance. General Trend: High Slug expression in various cancers (including breast, colorectal, head and neck, and others) is frequently correlated with a more aggressive phenotype and poorer clinical outcomes. |
| 4535- | MAG, | 5-FU, | Magnolol and 5-fluorouracil synergy inhibition of metastasis of cervical cancer cells by targeting PI3K/AKT/mTOR and EMT pathways |
| - | in-vitro, | Cerv, | NA |
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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