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| MOMP is the point-of-no-return decision step of intrinsic apoptosis. It is the event in which the mitochondrial outer membrane becomes permeable, allowing release of pro-death factors that irreversibly commit a cell to die. Cancer progression is characterized by systematic suppression, buffering, or decoupling of MOMP from lethal execution. MOMP occurs when BAX and/or BAK oligomerize in the mitochondrial outer membrane, forming pores that release: -Cytochrome c → apoptosome → caspase-9 -Smac/DIABLO → IAP neutralization -Other apoptogenic factors (e.g., Omi/HtrA2) Once sufficient mitochondria undergo MOMP, cell death is inevitable (even if caspases are later inhibited). Redox, Metabolism, and MOMP (Critical) -High xCT / GSH → suppress mitochondrial ROS → MOMP ↓ -Autophagic flux → removes damaged mitochondria → MOMP ↓ -Pro-oxidant overload → mitochondrial dysfunction → MOMP ↑ |
| 5378- | ART/DHA, | Natural Agents Modulating Ferroptosis in Cancer: Molecular Pathways and Therapeutic Perspectives |
| - | Review, | Var, | NA |
| 5130- | ART/DHA, | Dihydroartemisinin Induces Apoptosis in Human Bladder Cancer Cell Lines Through Reactive Oxygen Species, Mitochondrial Membrane Potential, and Cytochrome C Pathway |
| - | in-vitro, | Bladder, | T24/HTB-9 |
| 5125- | Sal, | Salinomycin induced ROS results in abortive autophagy and leads to regulated necrosis in glioblastoma |
| - | in-vitro, | GBM, | 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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