阿曼托双黄酮通过JAK2-STAT3通路影响甲状腺癌SW579细胞的增殖和凋亡  

Amentoflavone induces apoptosis and suppresses proliferation of thyroid carcinoma SW579 cells by inhibiting the activation of JAK2-STAT3 pathway

作　　者：马涛[1] 王红梅[2] 赵婷[1] 黄凌燕[3] 王瑞肖 MA Tao;WANG Hongmei;ZHAO Ting;HUANG Lingyan;WANG Ruixiao(Third Department of Surgical Oncology,General Hospital of Ningxia Medical University,Yinchuan 750004,Ningxia,China;Department of Pharmacology,School of Pharmacy,Southeast University,Nanjing 210000,Jiangsu,China;Department of Pathology,General Hospital of Ningxia Medical University,Yinchuan 750004,Ningxia,China)

机构地区：[1]宁夏医科大学总医院肿瘤外三科,宁夏银川750004 [2]东南大学药学院药理学系,江苏南京210000 [3]宁夏医科大学总医院病理科,宁夏银川750004

出　　处：《中国肿瘤生物治疗杂志》2023年第3期211-216,共6页Chinese Journal of Cancer Biotherapy

基　　金：国家自然科学基金(No.81602327)。

摘　　要：目的:探讨阿曼托双黄酮(AF)对甲状腺癌SW579细胞中JAK2-STAT3通路活化及其细胞增殖和凋亡的影响。方法:用0、50、100、150、200μmol/L的AF处理SW579细胞24、48、72 h,采用CCK-8和Celigo计数、FCM、WB及qPCR法检测AF对SW579细胞的增殖、凋亡、JAK2-STAT3通路活化及其下游调控基因c-Myc、Bcl2、survivin的mRNA及蛋白表达水平的影响。结果:AF处理后,SW579细胞增殖能力显著下降(P<0.05)且呈浓度依赖性,细胞凋亡呈浓度依赖性增多(P<0.05),细胞中JAK2-STAT3通路的活化受到显著抑制(P<0.05),其下游基因c-Myc、Bcl2、survivin的mRNA及蛋白表达均明显下降(均P<0.05)。结论:AF可通过抑制SW579细胞中JAK2-STAT3通路活化及其下游基因的表达而抑制SW579细胞的增殖并促进其凋亡,有望成为治疗甲状腺癌的有效药物。Objective:To investigate the effects of Amentoflavone(AF)on the JAK2-STAT3 pathway activation,apoptosis,and proliferation of thyroid carcinoma SW579 cells.Methods:SW579 cells were treated with AF at different concentrations(0,50,100,150,and 200μmol/L)for 24 h,48 h,and 72 h,respectively.Then,the effects of AF on the proliferation and apoptosis of SW579 cells were detected by CCK-8 and Celigo cell count and FCM,respectively;and the effects of AF on the JAK2-STAT3 pathway activation and the mRNA and protein expression of its downstream genes c-Myc,Bcl2 and Survivin in SW579 cells were detected by qPCR and Western blotting.Results:After the treatment with AF,the proliferation of SW579 cells was suppressed significantly while the apoptosis was promoted significantly,which were all in a dose-dependent manner(both P<0.05).The activation of JAK2-STAT3 pathway was significantly inhibited(P<0.05),and the mRNA and protein expression of the downstream genes c-Myc,Bcl2,and survivin in SW579 cells was significantly decreased(all P<0.05)after the treatment with AF.Conclusion:AF may contribute to apoptosis induction and proliferation suppression of thyroid carcinoma SW579 cells via inhibiting the activation of JAK2-STAT3 pathway and its downstream gene expression.AF has the potential to serve as a novel therapeutic approach for the management of thyroid carcinoma.

关 键 词：阿曼托双黄酮 甲状腺癌 SW579细胞 JAK2-STAT3 凋亡 增殖 

分 类 号：R736.1[医药卫生—肿瘤] R285[医药卫生—临床医学]