摘要
目的:采用动物实验和临床标本探讨白细胞介素-17A(IL-17A)对卵巢癌(OvCa)进展的影响,并探索相应机制。方法:以C57BL/6遗传背景的野生型(WT)小鼠和IL-17A缺陷型(IL-17A-/-)小鼠为研究对象,原位注射相同基因背景来源的小鼠OvCa细胞系ID8构建卵巢原位种植瘤模型,观察IL-17A对小鼠OvCa生长转移的影响。应用Western印迹检测WT小鼠和IL-17A-/-小鼠肿瘤组织中信号转导和转录激活因子3(STAT3)、磷酸化STAT3(p-STAT3)、脂肪酸结合蛋白4(FABP4)表达情况,以探讨IL-17A促进OvCa进展的机制。收集OvCa患者临床病理组织切片标本,应用免疫组化分析IL-17A、FABP4表达与OvCa进展的相关性。结果:WT小鼠造模部位卵巢明显肿大,与周围组织黏连,其表面可见若干瘤结节;IL-17A-/-小鼠卵巢肿大,与周围组织无黏连,表面瘤结节较少。与WT小鼠相比,IL-17A-/-小鼠腹腔瘤结节显著减少(t=5.132,P<0.05)。Western印迹结果显示与WT小鼠相比,IL-17A-/-小鼠肿瘤组织中p-STAT3、FABP4蛋白表达显著降低(均P<0.05)。OvCa患者临床病理标本显示IL-17A、FABP4表达与癌症FIGO分期、转移相关(均P<0.05),并且在OvCa患者中IL-17A与FABP4表达也具有一定相关性(P<0.05)。结论:动物实验和临床标本证实IL-17A通过上调FABP4表达促进OvCa进展。
Objective:Animal experiments and clinical specimens were applied to investigate the effect of interleukin-17A(IL-17A)on the progression of ovarian cancer(OvCa),and to explore the corresponding mechanism.Methods:Wild-type(WT)mice and IL-17Adeficient(IL-17A-/-)mice with C57BL/6 genetic background were used as the research objects,and the mouse OvCa cell line ID8 derived from the same genetic background was injected in situ to construct ovarian orthotopic tumor implantation model to observe the effect of IL-17A on the growth and metastasis of OvCa in mice.Western blotting was used to detect the expression of signal transducer and activator of transcription 3(STAT3),phosphorylated STAT3(p-STAT3)and fatty acid-binding protein 4(FABP4)in tumor tissues of WT mice and IL-17A-/-mice to explore the mechanism of IL-17A promoting OvCa progression.The clinicopathological specimens of OvCa patients were collected and immunohistochemistry was used to analyze the correlation between the expression of IL-17A,FABP4 and OvCa progression.Results:The ovaries of WT mice were obviously enlarged and adhered to the surrounding tissues,and several nodules were seen on the surface of the ovaries.The ovaries of IL-17A-/-mice were enlarged,without adhesion to the surrounding tissues,and there were few tumor nodules on the surface.Compared with WT mice,the tumor nodules in the peritoneal cavity of IL-17A-/-mice were significantly reduced(t=5.132,P<0.05).Western blotting showed that compared with WT mice,the protein expressions of p-STAT3 and FABP4 of tumor nodules in IL-17A-/-mice were significantly decreased(both P<0.05).The clinicopathological specimens of OvCa showed that the expression of IL-17A and FABP4 was correlated with FIGO stage and metastasis of cancer(both P<0.05),and the expression of IL-17A was also correlated with FABP4 in OvCa patients(P<0.05).Conclusion:Results of animal experiments and clinical specimens confirmed that IL-17A promoted OvCa progression by upregulating the expression of FABP4.
作者
郑小燕
郁春艳
刘俊汝
刘子璇
陈思琦
邓为民
ZHENG Xiao-yan;YU Chun-yan;LIU Jun-ru;LIU Zi-xuan;CHEN Si-qi;DENG Wei-min(Department of Immunology,School of Basic Medical Sciences,Tianjin Medical University,Key Laboratory of Diseases and Microenvironment of Ministry of Education of China,Tianjin 300070,China)
出处
《天津医科大学学报》
2023年第2期148-152,共5页
Journal of Tianjin Medical University
基金
国家自然科学基金(82273340)
京津冀基础研究合作专项(20JCZXJC00140)。
关键词
IL-17A
卵巢癌
FABP4
sovarian cancer
IL-17A
FABP4
progression of cancer
