| 邹渭洪，付成效，秦旭平.STAT4基因缺失增强髓系抑制性细胞动员促进小鼠炎症相关肠癌的发生.[J].中南医学科学杂志.,2014,42(4):343-347. |
| STAT4基因缺失增强髓系抑制性细胞动员促进小鼠炎症相关肠癌的发生 |
| Genetic Deficiency of STAT4 Promotes Inflammation Associated Colonic Carcinogenesis Through Increasing of Myeloid Derived Suppressor Cells |
| 投稿时间：2014-02-04 |
| DOI： |
| 中文关键词: 炎症 结肠癌 髓系抑制性细胞 信号转导与转录激活因子4 |
| 英文关键词:Inflammation,colon cancer,myeloid-derived suppressor cell (MDSC),signal transducer and activator of transcription 4 (STAT4) |
| 基金项目:湖南省科技厅项目（2012SK3153），国家自然科学基金资助项目（81173060）南华大学回国人员启动基金（2010XQD44）. |
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| 中文摘要: |
| 目的探索信号转导与转录因子4（STAT4）对髓系抑制性细胞（MDSCs）动员和分化的调控及其在结肠癌发生发展中的作用。方法应用信号转导与转录激活因子4基因敲除（STAT4-/-）小鼠建立炎症相关肠癌模型，STAT4-/-小鼠通过腹腔注射氧化偶氮甲烷(AOM)和饮用含DSS水诱发急性肠炎，建立炎症相关结肠肿瘤模型并鉴定；应用流式细胞技术分析STAT4基因缺失对免疫细胞亚群分化和动员的影响。结果STAT4-/-小鼠表现为明显的结肠肿瘤病变,而野生型（WT）对照组在结肠的中下段和肛门处只有炎性病变和上皮组织增生；CD11b+Gr-1+MDSCs在STAT4-/-小鼠的外周血、脾脏和骨髓内的百分率较WT对照组小鼠显著增加（P<0.05）。结论STAT4缺失能促进小鼠结肠肿瘤的发生，其机制可能与STAT4信号通路抑制导致CD11b+Gr-1+MDSCs的异常分化和动员有关。 |
| 英文摘要: |
| ObjectiveTo investigate the role of signal transducer and activator of transcription 4 (STAT4) signal pathway in the migration of Myeloid-derived suppressor cells (MDSCs) and in inflammation associated carcinogenesis.MethodsThe inflammation associated colon cancer mouse model was established with STAT4 genetic deficiency mice through administration of azoxymethane (AOM) and dextran sulfate sodium (DSS) treatment.Flow cytometery was performed to analyze the expression of CD11b+Gr-1+MDSCs in the peripheral blood,spleen,and bone marrow.ResultsGenetic deficiency of STAT4 showed colon tumorigenesis following AOM/DSS treatment.Significant increasing of CD11b+Gr-1+MDSCs was examined in the inflamed colon tissue and in the peripheral blood of STAT4-/- mice.Genetic deficiency of STAT4 promoted the proliferation and differentiation of CD11b+Gr-1+immature myeloid cells within bone marrow and spleen reservoirs.ConclusionsSTAT4 signal pathway plays a criticle role in regulating the differentiation and migration of CD11b+Gr-1+MDSCs that promotes inflammation associated colonic tumorigenesis. |
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