Compounds > 2-methylnaphtho(2-3-b)furan-4-9-dione

2-methylnaphtho(2-3-b)furan-4-9-dione and Adenocarcinoma

2-methylnaphtho(2-3-b)furan-4-9-dione has been researched along with Adenocarcinoma* in 1 studies

Other Studies

1 other study(ies) available for 2-methylnaphtho(2-3-b)furan-4-9-dione and Adenocarcinoma

Article	Year
Mitochondrial damage prior to apoptosis in furanonaphthoquinone treated lung cancer cells. Cancer detection and prevention, 2003, Volume: 27, Issue:1 The mechanisms of the antitumor reactions of 2-methylnaphtho[2,3-b]furan-4,9-dione (FNQ3) to human lung adenocarcinoma A549 cells were investigated. A549 cells that received 1.25 microg/ml FNQ3 (IC(50) at 0.35 microg/ml) developed intensive mitochondrial H(2)O(2) production at 1 h. Selective structural mitochondrial swelling, alteration of mitochondrial membrane potential, and cytochrome c and caspase-9 release from the mitochondria occurred 18-24 h later. alpha-Tocopherol inhibited the alteration of both mitochondrial permeability and the leakage of procaspase-9. The caspase-9 was then activated in the cytosol. The expression of Bcl-2 oncoprotein was suppressed by FNQ3, and resulted in apoptosis. The higher dose of 5 microg/ml induced necrosis via severe mitochondrial breakage. These results showed that FNQ3 targets the mitochondria of A549 cells to produce a reactive oxygen species resulting in apoptosis and necrosis. Topics: Adenocarcinoma; alpha-Tocopherol; Antineoplastic Agents, Phytogenic; Antioxidants; Apoptosis; Blotting, Western; Caspase 9; Caspases; Cytochrome c Group; Cytoplasm; DNA Fragmentation; Dose-Response Relationship, Drug; Electrophoresis, Polyacrylamide Gel; Flow Cytometry; Genes, bcl-2; Humans; Hydrogen Peroxide; Lung Neoplasms; Membrane Potentials; Microscopy, Confocal; Microscopy, Electron; Mitochondria; Naphthoquinones; Necrosis; Permeability; Tumor Cells, Cultured	2003

Article

Year

Mitochondrial damage prior to apoptosis in furanonaphthoquinone treated lung cancer cells.

Cancer detection and prevention, 2003, Volume: 27, Issue:1

The mechanisms of the antitumor reactions of 2-methylnaphtho[2,3-b]furan-4,9-dione (FNQ3) to human lung adenocarcinoma A549 cells were investigated. A549 cells that received 1.25 microg/ml FNQ3 (IC(50) at 0.35 microg/ml) developed intensive mitochondrial H(2)O(2) production at 1 h. Selective structural mitochondrial swelling, alteration of mitochondrial membrane potential, and cytochrome c and caspase-9 release from the mitochondria occurred 18-24 h later. alpha-Tocopherol inhibited the alteration of both mitochondrial permeability and the leakage of procaspase-9. The caspase-9 was then activated in the cytosol. The expression of Bcl-2 oncoprotein was suppressed by FNQ3, and resulted in apoptosis. The higher dose of 5 microg/ml induced necrosis via severe mitochondrial breakage. These results showed that FNQ3 targets the mitochondria of A549 cells to produce a reactive oxygen species resulting in apoptosis and necrosis.

Topics: Adenocarcinoma; alpha-Tocopherol; Antineoplastic Agents, Phytogenic; Antioxidants; Apoptosis; Blotting, Western; Caspase 9; Caspases; Cytochrome c Group; Cytoplasm; DNA Fragmentation; Dose-Response Relationship, Drug; Electrophoresis, Polyacrylamide Gel; Flow Cytometry; Genes, bcl-2; Humans; Hydrogen Peroxide; Lung Neoplasms; Membrane Potentials; Microscopy, Confocal; Microscopy, Electron; Mitochondria; Naphthoquinones; Necrosis; Permeability; Tumor Cells, Cultured

2003