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 4.0 μmol/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.