首页> 中文期刊> 《贵州医药》 >IL-10、STAT3在口腔鳞状细胞癌中表达与肿瘤相关巨噬细胞间的关系

IL-10、STAT3在口腔鳞状细胞癌中表达与肿瘤相关巨噬细胞间的关系

         

摘要

目的 探讨人口腔鳞状细胞癌(OSCC)组织中白细胞介素(IL-10)、信号传导与转录激活因子 3 (STAT3)与肿瘤相关巨噬细胞极化间的关系.方法 采用免疫组织化学法检测 IL-10、STAT3 蛋白含量、CD68+、CD163+巨噬细胞阳性标记物在肿瘤组织中、正常组织中的表达水平并分析其与临床病理指标之间的相互关系.结果 人口腔鳞状细胞癌组织中 IL-10、STAT3 蛋白的表达和 CD163+、CD68+巨噬细胞浸润数均显著高于正常组(P﹤0.05).STAT3、CD163+、CD68+在中低分化的表达高于高分化的表达(P﹤0.05).IL-10、STAT3、CD163+在临床分期中Ⅲ+Ⅳ期患者较Ⅰ+Ⅱ期患者多(P均﹤0.05).IL-10、STAT3、CD163+、CD68+在有淋巴结转移组较无淋巴结转移多(P均﹤0.05).癌组织中 IL-10、STAT3 的表达与CD1 6 3+巨噬细胞浸润数之间呈正相关(r1=0.347,r2=0.397,P﹤0.05).IL-10 与STAT3 的表达呈正相关(r=0.421,P﹤0.05 ).结论 口腔鳞癌中存在大量巨噬细胞浸润.M2 型巨噬细胞与口腔鳞癌的发生、浸润、转移有关,其机制可能与肿瘤环境中 IL-10 及 STAT3 高表达有关,IL-1 0 的表达上调激活 STAT3 可能使巨噬细胞更多向 M2 型转化,从而促进肿瘤的浸润与转移.%Objective To investigate the expressions of IL-10,STAT3,CD68 and CD163 in oral squamous cell carcinoma (OSCC)and its relationships between clinical characteristics and tumor-associated macrophage polariza-tion.Methods By immunohistochemically method to detect the expressions of IL-10,STAT3,CD68+ and CD163+ in 42 primary OSCC tumor tissues and 15 samples with normal tissues as the control group.The correlation between macrophages distribution and clinical pathological features was explored.ResultsIt was found that theexpression of IL-10,STAT3,CD163+,CD68+ were significantly higher than normal group(P﹤0.05).STAT3,CD163+,CD68+ protein positive phenotype patients in the middle and poor differentiated group were higher than well differentiated group,IL-10,STAT3,CD163+ in the clinical Ⅲ+Ⅳstage patients were more than the clinicalⅠ+Ⅱstagepatients. And the lymph node metastasis was significantly higher than that without lymph node metastasis in IL-10,STAT3, CD163+ and CD68(P﹤0.05),the number of M2 macrophages in OSCC was positively correlated with the expres-sions of IL-10,STAT3(r1=0.347,r2=0.397,P﹤0.05).IL-10 and STAT3 were positively correlated in OSCC(r=0.421,P﹤0.05).Conclusion M2 macrophage may be related with the occurrence,invasion and metastasis of OSCC, and IL-10,STAT3 suggesting a role for M2 macrophage polarization in this process and may participate in the devel-opment of OSCC.The upregulation of IL-10 activates STAT3 to make macrophages transform into M2 macropha-ges,so as to promote the infiltration and metastasis of tumor.

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