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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. |
| Lung CSC (Cancer Stem Cells) markers (CD133, CD44, ALDHA1, Nanog and Oct4) |
| 1565- | Api, | Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Nor, | BEAS-2B | - | in-vitro, | Lung, | H1975 |
| 566- | ART/DHA, | 2DG, | Dihydroartemisinin inhibits glucose uptake and cooperates with glycolysis inhibitor to induce apoptosis in non-small cell lung carcinoma cells |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Lung, | PC9 |
| 1524- | Ba, | Baicalein Induces Caspase‐dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells |
| - | in-vitro, | Lung, | A549 |
| 2476- | Ba, | Baicalein Induces Caspase-dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells |
| - | in-vitro, | Lung, | A549 |
| 1378- | BBR, | Berberine induces non-small cell lung cancer apoptosis via the activation of the ROS/ASK1/JNK pathway |
| - | in-vitro, | Lung, | NA |
| 5880- | CAR, | In vitro and in vivo antitumor potential of carvacrol nanoemulsion against human lung adenocarcinoma A549 cells via mitochondrial mediated apoptosis |
| - | vitro+vivo, | Lung, | A549 | - | in-vitro, | Nor, | BEAS-2B | - | in-vitro, | Lung, | PC9 |
| 6189- | Cuc, | Cucurbitacin B inhibits proliferation and induces apoptosis via STAT3 pathway inhibition in A549 lung cancer cells |
| - | in-vitro, | Lung, | A549 |
| 432- | CUR, | Curcumin-Induced Global Profiling of Transcriptomes in Small Cell Lung Cancer Cells |
| - | in-vitro, | Lung, | H446 |
| 1981- | CUR, | Mitochondrial targeted curcumin exhibits anticancer effects through disruption of mitochondrial redox and modulation of TrxR2 activity |
| - | in-vitro, | Lung, | NA |
| 1327- | EMD, | Emodin induces apoptosis in human lung adenocarcinoma cells through a reactive oxygen species-dependent mitochondrial signaling pathway |
| - | in-vitro, | Lung, | A549 |
| 835- | Gra, | Annona muricata leaves induced apoptosis in A549 cells through mitochondrial-mediated pathway and involvement of NF-κB |
| - | in-vitro, | Lung, | A549 |
| 2879- | HNK, | Honokiol Inhibits Lung Tumorigenesis through Inhibition of Mitochondrial Function |
| - | in-vitro, | Lung, | H226 | - | in-vivo, | NA, | NA |
| 1924- | JG, | Juglone triggers apoptosis of non-small cell lung cancer through the reactive oxygen species -mediated PI3K/Akt pathway |
| - | in-vitro, | Lung, | A549 |
| 2995- | PL, | Piperlongumine overcomes osimertinib resistance via governing ubiquitination-modulated Sp1 turnover |
| - | in-vitro, | Lung, | H1975 | - | in-vitro, | Lung, | PC9 | - | in-vivo, | NA, | NA |
| 3010- | RosA, | Exploring the mechanism of rosmarinic acid in the treatment of lung adenocarcinoma based on bioinformatics methods and experimental validation |
| - | in-vitro, | Lung, | A549 | - | in-vivo, | NA, | NA |
| 1002- | SSE, | Osi, | Adag, | Selenite as a dual apoptotic and ferroptotic agent synergizes with EGFR and KRAS inhibitors with epigenetic interference |
| - | in-vitro, | Lung, | H1975 | - | in-vitro, | Lung, | H385 |
| - | vitro+vivo, | Lung, | NA |
| 5079- | SSE, | Rad, | The solvent and treatment regimen of sodium selenite cause its effects to vary on the radiation response of human bronchial cells from tumour and normal tissues |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Nor, | BEAS-2B |
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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