Effect of sodium norcantharidate on the proliferation,apoptosis and inflammatory immune responses of gastric cancer cells in humans based on IL-6/JAK2/STAT3 pathway
Objective To determine the effect of sodium norcantharidate(SNCTD)on the proliferation,apoptosis and inflammatory immunity of gastric cancer cells,and the role of IL-6/JAK2/STAT3 pathway in these effects.Methods Human gastric cancer HGC-27 cells were used as objects.CCK-8 assay was used to measure the rate of cell proliferation inhibition after the treatment with various concentrations of SNCTD[0.25,0.5,1,2,4,8,and 16 μmol·L-1]for 24 and 48 h.After the treatment with various concentrations of SNCTD[1,2,and 4 μmol·L-1]for 24 h,ELISA was used to measure the concentration levels of IL-6 in the cell supernatant.Flow cytometry was used to measure the apoptosis rate of cells.Western blot and RT-qPCR were used to measure the expressions at mRNA and protein expressions of IL-6/JAK2/STAT3 pathway genes(IL-6,GP130,JAK2,STAT3)and the cell proliferation and apoptosis genes(c-Myc,Bcl-2,Bax)respectively.Results Compared with the control group,the growth inhibition rate and apoptosis rate of the SNCTD groups were significantly increased(P＜0.05).The level of IL-6 in the supernatant was decreased(P＜0.01).The mRNA and protein expression levels of c-Myc and Bcl-2 were significantly decreased(P＜0.05),while Bax mRNA and protein expression increased significantly(P＜0.05).The expressions of IL-6,GP130,p-JAK2/JAK2,and p-STAT3/STAT3 protein JAK2 and STAT3 mRNA was decreased(P＜0.05).Conclusion SNCTD can effectively inhibit the proliferation and induce the apoptosis of gastric cancer cells,whose mechanism of action may be connected with the fact that SNCTD can reduce the expression of inflammatory factor IL-6 in the tumor microenvironment.The activation of IL-6/JAK2/STAT3 signaling pathway is inhibited to regulate the transcription and translation of specific genes,namely down-regulating the expression of c-Myc and Bcl-2 and up-regulating the expression of Bax.
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