Quinalizarin induces apoptosis in gastric cancer AGS cells via MAPK and Akt signaling pathway
LIU Chang
LUO Yinghua
PIAO Xianji
WANG Yue
MENG Lingqi
WANG Hao
WANG Jiaru
ZHANG Yi
LI Jinqian
JIN Chenghao
Abstract：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 14.18μmol/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.
Keywords：quinalizaringastric cancer cellsapoptosisreactive oxygen speciescell signaling
Publication Date：2017-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：7( 1085-1091 )