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Chinese journal of cancer 2010-Mar

Effects of ternary complexes of copper with salicylaldehyde-amino acid Schiff base coordination compounds on the proliferation of BGC823 cells.

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Врската е зачувана во таблата со исечоци
Ai-Juan Guo
Xiao-Shan Xu
Ying-Hui Hu
Ming-Zhao Wang
Xin Tan

Клучни зборови

Апстракт

OBJECTIVE

The basic structure of salicylaldehyde-amino acid Schiff base compounds includes a C=N chemical bond. These compounds show significant antitumor activities in vitro when combined with a metal ion. This study investigated the effects and possible mechanisms of four salicylaldehyde-amino acid Schiff base copper ternary coordination compounds on the proliferation of human gastric cancer cell line BGC823.

METHODS

The BGC823 cells were treated with the four compounds (6B, 7B, 6P, and 7P). Cell proliferation was detected by MTT assay. Apoptosis and changes in the cell cycle were analyzed by flow cytometry. DNA damage was observed using a DNA ladder assay. The expression of p53 protein was determined by immunocytochemistry.

RESULTS

The proliferation of BGC823 cells was significantly inhibited by the four compounds and the effect was concentration-dependent. The half maximal inhibitory concentration (IC50) of 6B, 7B, 6P, and 7P for BGC823 cells were 18.10, 27.50, 3.61, and 3.45 micromol/L, respectively. Flow cytometry showed the four drugs induced apoptosis in BGC823 cells, which was confirmed by DNA ladder experiments. Flow cytometry also detected changed phases in the cell cycle from treatment with the compounds. The percent of cells in the G(0)/G(1) phase decreased and that of cells in the G1/S and G(2)/M phases increased, indicating that S-and G2-phase blockages exist. As shown by immunocytochemistry, the expression of p53 decreased in BGC823 cells treated with the four drugs, indicating the involvement of the p53 pathway to BGC823 cell apoptosis.

CONCLUSIONS

The four compounds showed significant activities on restraining proliferation of BGC823 cells in vitro, induced apoptosis, and caused changes in the cell cycle. This may be related to the downregulation of p53.

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