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| Cytochrome c ** The term "release of cytochrome c" ** an increase in level for the cytosol. Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis. The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis. In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death. Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation. Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol. The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death. On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer. On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells. Overexpressed in Breast, Lung, Colon, and Prostrate. Underexpressed in Ovarian, and Pancreatic. |
| Pancreatic Cancer: Hypoxia (low oxygen tension) is commonly found in solid tumors. Hypoxia-inducible factor-1 (HIF-1),is a key mediator of the cellular response to hypoxia and is overexpressed in a wide variety of solid tumors, including pancreatic cancer. Nanog is highly expressed in CSCs compared to normal cells [93–97] HIF-1↑ |
| 1563- | Api, | MET, | Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells |
| - | in-vitro, | Nor, | HDFa | - | in-vitro, | PC, | AsPC-1 | - | in-vitro, | PC, | MIA PaCa-2 | - | in-vitro, | Pca, | DU145 | - | in-vitro, | Pca, | LNCaP | - | in-vivo, | NA, | NA |
| 5836- | CAP, | In vitro and in vivo induction of apoptosis by capsaicin in pancreatic cancer cells is mediated through ROS generation and mitochondrial death pathway |
| - | vitro+vivo, | PC, | AsPC-1 | - | in-vitro, | PC, | Bxpc-3 |
| 2014- | CAP, | Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells |
| - | in-vitro, | PC, | Bxpc-3 | - | in-vitro, | Nor, | HPDE-6 | - | in-vivo, | PC, | AsPC-1 |
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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