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Arsenic trioxide induces apoptosis of gastric cancer cell AGS and influences STAT3 and VEGF expression
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Abstract:
To investigate the apoptosisinducing effect of arsenic trioxide (As2O3) on gastric carcinoma cell line AGS in vitro and to assess the influence of As2O3 on the expression of signal transducers and activators of transcription 3 (STAT3) and vascular endothelial growth factor (VEGF). Methods: AGS cells were treated with different concentrations of As2O3 (1, 5, and 10 μmol/L) for 24,48, and 72 h. The cell proliferation was detected by MTT assay, cell apoptosis and cell cycle distribution were measured by flow cytometry and TUNEL, and the expression of STAT3 and VEGF was investigated by ELISA, immunohistochemistry and realtime PCR. Results: (1) As2O3 inhibited AGS cell proliferation in a time and dosedependent manner; (2) FCM results showed a typical subdiploid peak before G0/ G1 phase and cell cycle analysis showed G2/M phase arrest; (3) TUNEL analysis revealed the DNA fragmentation; (4) During the As2O3induced apoptosis of AGS cells, the expression of STAT3 and VEGF was downregulated, especially when As2O3 was at 10 mol/L. Conclusion: As2O3 can inhibit the proliferation of AGS cells and induce AGS cell apoptosis, which might be related with cell cycle block and downregulation of STAT3 and VEGF expression.
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