Effects of HIF-1α on human gastric cancer cell apoptosis at different CO2 pressures

The effects and potential molecular mechanisms underlying carbon dioxide (CO2) pneumoperitoneum on gastric cancer cell apoptosis are not fully understood. In this study, we assessed the effects of CO2 pneumoperitoneum on the apoptosis of MKN-45 gastric cancer cells. Additionally, we investigated the role of HIF-1α in CO2 pneumoperitoneum-induced apoptosis of gastric cancer cells. MKN-45 cells were cultured in CO2 or air pneumoperitoneum at 0, 12 and 15 mmHg pressures for 4 h. We observed a change in cells morphology and increasing apoptotic ratios in MKN-45 cells when they were put into a 15 mmHg CO2 pneumoperitoneum environment. However, there was no significant difference between the 0, 12 mmHg CO2 pneumoperitoneum and the control groups. Exposure to 15 mmHg CO2 pneumoperitoneum significantly enhanced the expression levels of HIF-1α and Bax, while it attenuated Bcl-2 expression levels. When we inhibited HIF-1α by small interfering RNA (siRNA), we found that the apoptotic ratio of MKN-45 cells decreased in 15 mmHg CO2 pneumoperitoneum. This treatment markedly elevated Bcl-2 levels and decreased Bax expression. These data suggest that CO2 pneumoperitoneum may accelerate the apoptosis of MKN-45 cells at higher pressures. HIF-1α is a crucial factor that affects gastric cancer cell apoptosis by downregulating the Bcl-2/Bax ratio.