Inhibitory effects of periplocin from cortex periplocae on proliferation of human esophageal carcinoma TE-13 cells
10.3781/j.issn.1000-7431.2008.03.006
- Author:
Lian-Mei ZHAO
1
Author Information
1. Research Center
- Publication Type:Journal Article
- Keywords:
Antineoplastic drugs (TCD);
Cell growth processes;
Cortex periplocan;
Cyclin dependent kinases;
Esophageal neoplasms
- From:
Tumor
2008;28(3):203-206
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To study the inhibitory effects of periplocin from cortex periplocae (CPP) on proliferation of human esophageal carcinoma TE-13 cells and the related mechanism for cell cycle arrest. Methods: The inhibitory effects of CPP on the growth of TE-13 cells were measured by MTT assay. The morphological changes of TE-13 cells were analyzed by Gimsa staining. Detection of cell apoptosis and cell cycles were performed by flow cytometry. Protein expressions of cyclin-dependent kinase CDK2 and CDK4 were analyzed by Western blotting assay. Results:CPP significantly inhibited the proliferation of TE-13 cells in a dose- and time-dependent manner (P < 0.01). After treatment with CPP for 48 h, the IC50 was 0.61 μg/mL. TE-13 cells showed morphologic changes of apoptosis after treatment with CPP 2 μg/mL for 48 h. The proportion of cells in G0/G1 phase significantly increased (P < 0.01) and the number of cells in S phase decreased (P < 0.01). The proportion of cells in G2/M phase had no significant difference before and after CPP treatment (P > 0.05). CDK4 expression was inhibites by CPP at different concentrations, but the expression of CDK2 had no marked changes (P > 0.05). Conclusion: CPP significantly inhibites the growth of TE-13 cells. The action mechanism may be related with induction of cell cycle blocking and apoptosis.
