Effects of Sodium Cantharidinate on Proliferation and Apoptosis of Gastric Cancer Cells by Inhibiting JAK2/STAT3 Pathway
Objective To study the effects of sodium cantharidinate (SC) on the proliferation and apoptosis of gastric cancer cells through JAK2/STAT3 pathway. Methods Gastric cancer cell line SGC-7901 was cultured and treated with different concentrations of SC (0.25,0.5,1.0,2.0,4.0,8.0,and 16.0 μmol/L) and then transfected with control plasmid or JAK2 plasmid. Cell survival rate,apoptosis rate,and the expression levels of p-JAK2,p-STAT3,p-p38,p-ERK,and p-JNK were detected after 48 h of treatment. Results The results indicated that 1.0,2.0,4.0,8.0,and 16.0 μmol/L of SC inhibited cell proliferation,and the survival rate decreased with an increase in SC concentration (P<0.05). SC doses of 1.0,2.0,and 4.0 μmol/L were selected for the subsequent experiments. Compared with the control group,the apoptosis rate of the 1.0 μmol/L SC group exhibited no significant difference (P>0.05),while those of the 2.0 and 4.0 μmol/L SC groups increased significantly (P<0.05). The expression levels of p-JAK2 and p-STAT3 significantly decreased (P<0.05),while no significant difference was noted in the expression levels of p-p38,p-ERK,and p-JNK (P>0.05) in the 1.0,2.0,and 4.0 μmol/L SC groups. The JAK2 plasmid was transfected simultaneously with the 4.0μmol/L SC treatment;the expression levels of p-JAK2 and p-STAT3 and the survival rate increased,whereas the apoptosis rate decreased (P<0.05). Conclusion SC inhibits the growth and promotes the apoptosis of gastric cancer cells,and its mechanism may be related to the inhibition of JAK2/STAT3 pathway activation.
万方数据
维普
