摘要
Regular use of aspirin （ASA） could reduce the risk of gastric cancer although the precise mechanism remains unclear. Down-regulation of survivin may be one of the cyclooxygenase-independent mechanisms whereby ASA induces apoptosis of gastric cancer cell. In this study, we investigated the effect of ASA on the growth, apoptosis and survivin expression of gastric cancer cell line SGC7901. The survival of cells treated with 3.0 and 10.0 mmol/L ASA for 24 h was decreased by 44.6% and 88.5%, respectively. ASA at 3.0 mmol/L inhibited the viability of SGC7901 cells in a time-dependent manner. Apoptosis analysis showed similar results with MTT assay. ASA at 3.0 and 10.0 mmol/L decreased the mRNA transcript levels of survivin and reduced survivin protein levels in SGC7901 cells also in a time-dependent manner. Our findings indicated that ASA inhibited the proliferation of SGC7901 by suppressing survivin at both the transcriptional and translational level.
Regular use of aspirin （ASA） could reduce the risk of gastric cancer although the precise mechanism remains unclear. Down-regulation of survivin may be one of the cyclooxygenase-independent mechanisms whereby ASA induces apoptosis of gastric cancer cell. In this study, we investigated the effect of ASA on the growth, apoptosis and survivin expression of gastric cancer cell line SGC7901. The survival of cells treated with 3.0 and 10.0 mmol/L ASA for 24 h was decreased by 44.6% and 88.5%, respectively. ASA at 3.0 mmol/L inhibited the viability of SGC7901 cells in a time-dependent manner. Apoptosis analysis showed similar results with MTT assay. ASA at 3.0 and 10.0 mmol/L decreased the mRNA transcript levels of survivin and reduced survivin protein levels in SGC7901 cells also in a time-dependent manner. Our findings indicated that ASA inhibited the proliferation of SGC7901 by suppressing survivin at both the transcriptional and translational level.
基金
supported by the Science Foundation of Jiangsu Province for Institutions of Higher Learning (No. 08kjb320004)
