The synthesized 2-(2-fluorophenyl)-6,7-methylenedioxyquinolin-4-one (CHM-1) promoted G2/M arrest through inhibition of CDK1 and induced apoptosis through the mitochondrial-dependent pathway in CT-26 murine colorectal adenocarcinoma cells

@article{Chou2009TheS2,
  title={The synthesized 2-(2-fluorophenyl)-6,7-methylenedioxyquinolin-4-one (CHM-1) promoted G2/M arrest through inhibition of CDK1 and induced apoptosis through the mitochondrial-dependent pathway in CT-26 murine colorectal adenocarcinoma cells},
  author={Li-Chen Chou and Jai-Sing Yang and Li‐Jiau Huang and Hsi-Chin Wu and Chi-Cheng Lu and Jo-Hua Chiang and Kuan-Tin Chen and Sheng-Chu Kuo and Jing-Gung Chung},
  journal={Journal of Gastroenterology},
  year={2009},
  volume={44},
  pages={1055-1063}
}
BackgroundIn this study, we investigated the effects of 2-(2-fluorophenyl)-6,7-methylenedioxyquinolin-4-one (CHM-1) on cell viability, cell cycle arrest and apoptosis in CT-26 murine colorectal adenocarcinoma cells.MethodsFor determining cell viability, the MTT assay was used. CHM-1 promoted G2/M arrest by PI staining and flow cytometric analysis. Apoptotic cells were evaluated by DAPI staining. We used CDK1 kinase assay, Western blot analysis and caspase activity assays for examining the CDK1… Expand
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