摘要
目的 探讨甘草查尔酮A对结直肠癌细胞恶性行为的影响,分析其作用机制是否与调控蛋白酪氨酸激酶2(JAK2)/信号转导子与激活子3(STAT3)信号通路有关.方法 用细胞计数试剂盒(CCK-8)、Transwell实验、流式细胞术和Western blot检测不同浓度(0、5、10、20 nmol/ml)甘草查尔酮A对结直肠癌细胞LoVo增殖、迁移、凋亡以及p-JAK2和p-STAT3蛋白水平的影响.用AG490抑制JAK2/STAT3信号通路,通过CCK-8、Transwell实验和流式细胞术评估LoVo细胞增殖、迁移、凋亡.结果 5、10、20 nmol/ml的甘草查尔酮A处理LoVo细胞48 h和72 h后的A450值、凋亡率显著升高(P＜0.05),迁移数以及p-JAK2和p-STAT3蛋白水平显著降低(P＜0.05).AG490处理LoVo细胞48 h和72 h后的A450值、凋亡率显著升高(P＜0.05),迁移数以及p-JAK2和p-STAT3蛋白水平显著降低(P＜0.05).AG490和甘草查尔酮A联合处理LoVo细胞48 h和72 h后的A450值、凋亡率显著升高(P＜0.05),迁移数显著降低(P＜0.05).结论 甘草查尔酮A通过抑制JAK2/STAT3信号通路来抑制结直肠癌细胞增殖和迁移,并促进细胞凋亡.
Abstract
Objective To investigate the impact of licochalcone A on the malignant behavior of colorectal cancer cells,and further to analyze whether the mechanism was related to the regulation of protein tyrosine kinase 2(JAK2)/signal transducer and activator 3(STAT3)signaling pathway.Methods CCK-8,Transwell experiment,flow cytometry and Western blot were used to detect the effect of licochalcone A at different concentrations(0,5,10,20 nmol/ml)on the proliferation,migration and apopto-sis and also p-JAK2 and p-STAT3 protein levels of colorectal cancer cell LoVo.AG490 was used to inhibit the JAK2/STAT3 sig-naling pathway,and the proliferation,migration,and apoptosis rate of LoVo cells were evaluated by CCK-8,Transwell experiment and flow cytometry.Results After treatment with 5,10,and 20 nmol/ml licochalcone A,the A450 value(48,72 h)and apoptosis rate of LoVo cells were significantly increased(P＜0.05),and migration number and the protein levels of p-JAK2 and p-STAT3 were significantly reduced(P＜0.05).After AG490 treatment,the A450 value(48,72 h)and apoptosis rate of LoVo cells were sig-nificantly increased(P＜0.05),and the migration number and the protein levels of p-JAK2 and p-STAT3 were significantly re-duced(P＜0.05).After the combined treatment of AG490 and licochalcone A,the A450 value(48,72 h)and apoptosis rate of Lo-Vo cells were significantly increased(P＜0.05),and the migration number was significantly reduced(P＜0.05).Conclusion licochalcone A inhibits the proliferation and migration of colorectal cancer cells and increases cell apoptosis through inhibiting the JAK2/STAT3 signaling pathway.
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