存在于肿瘤微环境的肿瘤相关巨噬细胞（TAM）的M1/M2表型转化可介导肿瘤免疫逃逸，但TAM表型转化机制仍未阐明。课题组发现： M1型巨噬细胞高表达长链非编码RNA-Xist及TAM表型转化调控关键因子C/EBP-α、KLF6，低表达miR-181a； miR-181a可促进TAM-M2表型转化，信息学预测miR-181a以相同的MRE与Xist和C/EBP-α/KLF6结合。那么Xist是否作为ceRNA竞争性调控C/EBP-α/KLF6介导的TAM表型转化？本课题拟在明确Xist与miR-181a特异结合基础上，检测并比较分别干预及相互干预Xist与miR-181a时TAM表型改变与C/EBP-α/KLF6改变的相关性，阐明Xist作为ceRNA竞争性参与miR-181a调控C/EBP-α/KLF6介导的TAM表型转化的作用与机制。为深入研究TAM表型转化机制提供新思路和新靶点。

The phenotypic switch in tumor-associated macrophage (TAM) mediates immunity escape of carcinoma, however, the underlying mechanisms in the phenotype switch of TAMs are still unclear. Our group found that TAM-M1 highly expressed Xist, a long non-coding RNA (LncRNA), and increased the expression of C/EBP-α, KLF6, but decreased the express of miR-181a. We also found that miR-181a induces macrophage polarized to M2 Phenotype. Bioinformatic analysis showed that miR-181a combined with Xist, C/EBP-α and KLF6 depending on the same microRNA response elements(MREs) .Therefore, can we presume that Xist regulates TAM phenotype switch mediated by C/EBP-α and KLF6 as a ceRNA? We plan to detect and analyze the changes and differences of TAM phenotype switch and the expressions of C/EBP-α and KLF6 after we interfere the expression of Xist and miR-181a respectively and alternately, after confirming the direct binding between Xist and miR-181a at endogenous levels. Our study will clarify the mechanism of Xist regulating TAM phenotype switch mediated by C/EBP-α and KLF6 as a ceRNA, and will propose a new target for deep researching the mechanism of maintaining TAM phenotype switch.