Baicalein Induced Cell Cycle Arrest and Apoptosis in Human Lung Squamous Carcinoma CH27 Cells

• Published in: Anticancer research 2005-03, Vol.25 (2A), p.959-964
• Main Authors: LEE, Hong Z, LEUNG, Henry Wing C, LAI, Miao Y, WU, Chun H
• Format: Article
• Language: English
• Subjects: Apoptosis - drug effects; Biological and medical sciences; Carcinoma, Squamous Cell - drug therapy; Carcinoma, Squamous Cell - metabolism; Carcinoma, Squamous Cell - pathology; Caspase 3; Caspases - metabolism; CDC2-CDC28 Kinases - metabolism; Cell Cycle - drug effects; Cell Line, Tumor; Cyclin B - metabolism; Cyclin B1; Cyclin D1 - metabolism; Cyclin-Dependent Kinase 2; Cyclin-Dependent Kinase 4; Cyclin-Dependent Kinases - metabolism; Dose-Response Relationship, Drug; Flavanones - pharmacology; Humans; Lung Neoplasms - drug therapy; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Medical sciences; Pneumology; Proto-Oncogene Proteins - metabolism; Proto-Oncogene Proteins c-bcl-2 - metabolism; S Phase - drug effects; Tumors; Tumors of the respiratory system and mediastinum
• ISSN: 0250-7005; 1791-7530

Baicalein, a flavonoid compound, is one of the active constituents of the root of Scutellariae Radix. Baicalein inhibited the growth of human lung squamous carcinoma CH27 cells in a dose-dependent manner. Cell cycle analysis revealed an increase in the S-phase cell population following 24-h exposure to 50 μM baicalein. During the S-phase arrest, analysis of cell cycle regulatory molecules demonstrated that baicalein decreased the levels of cdk 4, cyclin B1 and cyclin D1. Furthermore, baicalein (50 μM) significantly induced cell apoptosis after 3 days of treatment. Baicalein induced apoptosis, as confirmed by condensed nuclei and DNA fragmentation, in CH27 cells. Baicalein-induced apoptosis was also accompanied by a decrease in Bcl-2 and caspase-3 proform levels. These results suggest that baicalein inhibits the proliferation of CH27 cells via S-phase arrest and apoptosis.