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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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| Source: HalifaxProj (inhibit) CGL-Driver Genes |
| Type: Antiapoptotic Oncogene |
| The proteins of BCL-2 family are classified into three subgroups, i.e., the anti-apoptotic/pro-survival proteins represented by BCL-2 and BCL-XL, the pro-apoptotic proteins represented by BAX and Bak, and the pro-apoptotic BH3-only proteins represented by BAD and BID. Since the expression of Bcl-2 protein in tumor cells is much higher than that in normal cells, inhibitors targeting it have little effect on normal cells. |
| - | in-vitro, | CRC, | HCT116 | - | in-vitro, | CRC, | LoVo | - | in-vivo, | CRC, | HCT116 |
| 4531- | MAG, | Magnolol-induced apoptosis in HCT-116 colon cancer cells is associated with the AMP-activated protein kinase signaling pathway |
| - | in-vitro, | CRC, | HCT116 |
| 4527- | MAG, | Magnolol inhibits growth and induces apoptosis in esophagus cancer KYSE-150 cell lines via the MAP kinase pathway |
| - | in-vitro, | ESCC, | TE1 | - | in-vitro, | ESCC, | Eca109 | - | vitro+vivo, | SCC, | KYSE150 |
| 4534- | MAG, | Molecular mechanisms of apoptosis induced by magnolol in colon and liver cancer cells |
| - | in-vitro, | Liver, | HepG2 | - | in-vitro, | CRC, | COLO205 |
| 4518- | MAG, | Cisplatin, | Evaluating the Magnolol Anticancer Potential in MKN-45 Gastric Cancer Cells |
| - | in-vitro, | GC, | MKN45 |
| 1314- | MAG, | Magnolol induces apoptosis via activation of both mitochondrial and death receptor pathways in A375-S2 cells |
| - | in-vitro, | Melanoma, | A375 |
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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