OBJECTIVE: To investigate quinalizarin-induced apoptosis in gastric cancer cells in vitro and explore the molecular mechanisms. METHODS: MTT assay was used to determine the cytotoxic effects of quinalizarin on human gastric cancer AGS, MKN-28 and MKN-45 cells. Annexin V-FITC/PI staining and flow cytometry were used to assess quinalizarin-induced apoptosis in AGS cells and its effect on intracellular ROS levels; the expression levels of apoptotic proteins in the cells were determined with Western blotting. RESULTS: Quinalizarin dose-dependently reduced the cell viabilities of the 3 gastric cancer cells (P<0.05). The IC50 values of quinalizarin in AGS, MKN-28 and MKN-45 cells were 7.07 µmol/L, 22.55 µmol/L and 14.18 µmol/L, respectively. Quinalizarin time-dependently induced apoptosis of AGS cells and potentiated the generation of intracellular reactive oxygen species (ROS) levels. Pretreatment with NAC, a scavenger of ROS, inhibited quinalizarin-induced apoptosis (P<0.001). Western blotting results showed that quinalizarin also up-regulated the expression levels of the apoptotic proteins including p-p38, p-JNK, Bad, cleaved caspase-3, and cleaved PARP-1 (P<0.05), and down-regulated the expression of the anti-apoptotic proteins p-Akt, p-ERK, and Bcl-2 (P<0.05). CONCLUSION: Quinalizarin inhibits the proliferation and induces apoptosis in gastric cancer cells in vitro through regulating intracellular ROS levels via the MAPK and Akt signaling pathways.
OBJECTIVE: To investigate quinalizarin-induced apoptosis in gastric cancer cells in vitro and explore the molecular mechanisms. METHODS:MTT assay was used to determine the cytotoxic effects of quinalizarin on humangastric cancer AGS, MKN-28 and MKN-45 cells. Annexin V-FITC/PI staining and flow cytometry were used to assess quinalizarin-induced apoptosis in AGS cells and its effect on intracellular ROS levels; the expression levels of apoptotic proteins in the cells were determined with Western blotting. RESULTS:Quinalizarin dose-dependently reduced the cell viabilities of the 3 gastric cancer cells (P<0.05). The IC50 values of quinalizarin in AGS, MKN-28 and MKN-45 cells were 7.07 µmol/L, 22.55 µmol/L and 14.18 µmol/L, respectively. Quinalizarin time-dependently induced apoptosis of AGS cells and potentiated the generation of intracellular reactive oxygen species (ROS) levels. Pretreatment with NAC, a scavenger of ROS, inhibited quinalizarin-induced apoptosis (P<0.001). Western blotting results showed that quinalizarin also up-regulated the expression levels of the apoptotic proteins including p-p38, p-JNK, Bad, cleaved caspase-3, and cleaved PARP-1 (P<0.05), and down-regulated the expression of the anti-apoptotic proteins p-Akt, p-ERK, and Bcl-2 (P<0.05). CONCLUSION:Quinalizarin inhibits the proliferation and induces apoptosis in gastric cancer cells in vitro through regulating intracellular ROS levels via the MAPK and Akt signaling pathways.
Authors: Lin Jiang; Le Wang; Lei Chen; Guo-Hong Cai; Qin-You Ren; Jian-Zong Chen; Heng-Jun Shi; Yong-Hong Xie Journal: Int J Clin Exp Med Date: 2015-02-15