摘要
目的 研究斑螯酸钠(SC)通过JAK2/STAT3通路对胃癌细胞增殖及凋亡的调控作用.方法 用不同浓度SC(0.25、0.5、1.0、2.0、4.0、8.0、16.0μmol/L)处理胃癌细胞株SGC-7901,转染对照质粒或JAK2质粒.处理48 h后检测细胞存活率、凋亡率及p-JAK2、p-STAT3、p-p38、p-ERK、p-JNK的表达水平.结果 1.0、2.0、4.0、8.0、16.0μmol/L SC处理后,胃癌SGC-7901细胞增殖受到抑制.随着SC浓度增加,细胞存活率降低(P<0.05);选择SC剂量1.0、2.0、4.0μmol/L进行后续实验.与对照组比较,1.0μmol/L SC组的细胞凋亡率无显著变化(P>0.05),2.0、4.0μmol/L SC组的细胞凋亡率显著增加(P<0.05);1.0、2.0、4.0μmol/L SC组的p-JAK2、p-STAT3表达水平显著降低(P<0.05),p-p38、p-ERK、p-JNK的表达水平无显著变化(P>0.05);4.0μmol/L SC处理的同时转染JAK2质粒,细胞中p-JAK2、p-STAT3的表达水平及细胞存活率增加、凋亡率降低(P<0.05).结论 SC能抑制胃癌SGC-7901细胞生长、促进胃癌细胞凋亡,其机制可能与抑制JAK2/STAT3通路激活有关.
Abstract
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.
维普
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