cgs-24012 and Lung-Neoplasms

cgs-24012 has been researched along with Lung-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for cgs-24012 and Lung-Neoplasms

Article	Year
DPMA, a deoxypodophyllotoxin derivative, induces apoptosis and anti-angiogenesis in non-small cell lung cancer A549 cells. Bioorganic & medicinal chemistry letters, 2013, Dec-15, Volume: 23, Issue:24 We found that the deoxypodophyllotoxin derivative, 2,6-dimethoxy-4-(6-oxo-(5R,5aR,6,8,8aR,9-hexahydrofuro[3',4':6,7]naphtho[2,3-d][1,3]dioxol-5-yl)phenyl ((R)-1-amino-4-(methylthio)-1-oxobutan-2-yl)carbamate (DPMA), exhibited superior cytotoxicity compared with etoposide. In this study, we investigated the mechanism of action of DPMA. DPMA exhibited anti-proliferative activity and induced apoptosis in A549 cells in a dose- and time-dependant manner. DPMA inhibited microtubule formation and induced expression of Bax, cleaved caspase-3, p53 and ROS, and inhibited Bcl-2 expression. DPMA also affected cyclinB1, cdc2 and p-cdc2 expression, inducing cell cycle arrest. DPMA also inhibited tube formation of VEGF-induced human umbilical vein endothelial cells. These studies demonstrate that DPMA inhibits p53/cdc2/Bax signaling, thereby inhibiting cell growth/angiogenesis and inducing apoptosis. Topics: Adenosine; Apoptosis; bcl-2-Associated X Protein; Carcinoma, Non-Small-Cell Lung; CDC2 Protein Kinase; Cell Cycle Checkpoints; Cell Line, Tumor; Drugs, Chinese Herbal; Human Umbilical Vein Endothelial Cells; Humans; Lung Neoplasms; Neovascularization, Physiologic; Podophyllotoxin; Signal Transduction; Tumor Suppressor Protein p53; Vascular Endothelial Growth Factor A	2013

Article

Year

DPMA, a deoxypodophyllotoxin derivative, induces apoptosis and anti-angiogenesis in non-small cell lung cancer A549 cells.

Bioorganic & medicinal chemistry letters, 2013, Dec-15, Volume: 23, Issue:24

We found that the deoxypodophyllotoxin derivative, 2,6-dimethoxy-4-(6-oxo-(5R,5aR,6,8,8aR,9-hexahydrofuro[3',4':6,7]naphtho[2,3-d][1,3]dioxol-5-yl)phenyl ((R)-1-amino-4-(methylthio)-1-oxobutan-2-yl)carbamate (DPMA), exhibited superior cytotoxicity compared with etoposide. In this study, we investigated the mechanism of action of DPMA. DPMA exhibited anti-proliferative activity and induced apoptosis in A549 cells in a dose- and time-dependant manner. DPMA inhibited microtubule formation and induced expression of Bax, cleaved caspase-3, p53 and ROS, and inhibited Bcl-2 expression. DPMA also affected cyclinB1, cdc2 and p-cdc2 expression, inducing cell cycle arrest. DPMA also inhibited tube formation of VEGF-induced human umbilical vein endothelial cells. These studies demonstrate that DPMA inhibits p53/cdc2/Bax signaling, thereby inhibiting cell growth/angiogenesis and inducing apoptosis.

Topics: Adenosine; Apoptosis; bcl-2-Associated X Protein; Carcinoma, Non-Small-Cell Lung; CDC2 Protein Kinase; Cell Cycle Checkpoints; Cell Line, Tumor; Drugs, Chinese Herbal; Human Umbilical Vein Endothelial Cells; Humans; Lung Neoplasms; Neovascularization, Physiologic; Podophyllotoxin; Signal Transduction; Tumor Suppressor Protein p53; Vascular Endothelial Growth Factor A

2013