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

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

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

Other Studies

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

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
Induced apoptosis and necrosis by 2-methylfuranonaphthoquinone in human cervical cancer HeLa cells. Cancer detection and prevention, 2000, Volume: 24, Issue:3 2-Methylnaphtho[2,3-b]furan-4,9-dione (FNQ3) has been reported to be more cytotoxic to human malignant tumor cell lines than are the corresponding normal epithelial cells. Therefore, we examined the dose response of FNQ3 against human cervical cancer HeLa cells in culture. When 1.25 mg/ml FNQ3 was applied, apoptosis was induced, as determined by an immunohistochemical staining of fragmented genome DNA and cell profiles. Significant inhibition of Bcl-2 oncogene protein expression by the same concentration of FNQ3 also was demonstrated by an immunohistochemical staining method to visualize the expressed cells and Western blot in polyacrylamide gel electrophoresis. Flow-cytometric spectra showed S-phase arrest in cell cycles and the appearance of sub-G1 phase consistent with apoptosis. On the other hand, concentrations of 5 microg/ml or more of FNQ3 induced necrosis. These results show that FNQ3 may act as an antitumor agent to induce apoptosis by affecting Bcl-2 expression and cell cycles, or necrosis as the result of primary mitochondrial injuries. Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Blotting, Western; Cell Cycle; Cervix Uteri; DNA; Dose-Response Relationship, Drug; Electrophoresis, Polyacrylamide Gel; Epithelial Cells; Female; Flow Cytometry; HeLa Cells; Humans; Immunohistochemistry; Mitochondria; Naphthoquinones; Necrosis; Proto-Oncogene Proteins c-bcl-2; S Phase; Time Factors; Uterine Cervical Neoplasms	2000

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

Induced apoptosis and necrosis by 2-methylfuranonaphthoquinone in human cervical cancer HeLa cells.

Cancer detection and prevention, 2000, Volume: 24, Issue:3

2-Methylnaphtho[2,3-b]furan-4,9-dione (FNQ3) has been reported to be more cytotoxic to human malignant tumor cell lines than are the corresponding normal epithelial cells. Therefore, we examined the dose response of FNQ3 against human cervical cancer HeLa cells in culture. When 1.25 mg/ml FNQ3 was applied, apoptosis was induced, as determined by an immunohistochemical staining of fragmented genome DNA and cell profiles. Significant inhibition of Bcl-2 oncogene protein expression by the same concentration of FNQ3 also was demonstrated by an immunohistochemical staining method to visualize the expressed cells and Western blot in polyacrylamide gel electrophoresis. Flow-cytometric spectra showed S-phase arrest in cell cycles and the appearance of sub-G1 phase consistent with apoptosis. On the other hand, concentrations of 5 microg/ml or more of FNQ3 induced necrosis. These results show that FNQ3 may act as an antitumor agent to induce apoptosis by affecting Bcl-2 expression and cell cycles, or necrosis as the result of primary mitochondrial injuries.

Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Blotting, Western; Cell Cycle; Cervix Uteri; DNA; Dose-Response Relationship, Drug; Electrophoresis, Polyacrylamide Gel; Epithelial Cells; Female; Flow Cytometry; HeLa Cells; Humans; Immunohistochemistry; Mitochondria; Naphthoquinones; Necrosis; Proto-Oncogene Proteins c-bcl-2; S Phase; Time Factors; Uterine Cervical Neoplasms

2000