肿瘤微环境是影响肿瘤侵袭转移的重要因素。肿瘤细胞与微环境中基质细胞互为调控、相互影响，共同参与肿瘤的发生发展。研究发现，S100蛋白与恶性肿瘤关系密切，在肿瘤细胞与肿瘤微环境的调控网络中发挥重要作用。我们前期研究发现，S100A7作为EF手相钙结合蛋白家族的成员，不仅可通过结合RAGE、激活ERK信号通路在肿瘤细胞内发挥促进肿瘤侵袭和转移的作用，而且可通过分泌至细胞外调控肿瘤微环境增强肿瘤细胞的侵袭转移能力。本研究拟在前期研究的基础上，系统深入地研究S100A7在宫颈癌肿瘤微环境调节中的作用，以及肿瘤细胞和肿瘤相关巨噬细胞、成纤维细胞相互调控的功能蛋白网络，进一步从整体水平动态评价S100A7参与宫颈癌转移的生物学功能和分子机理。本研究为进一步揭示宫颈癌转移的分子机制，探索宫颈癌转移相关的新的肿瘤标记分子和潜在的治疗靶点提供依据。

Tumor Microenvironment (TME) is closely associated with the malignant progression of tumors in its invasion and metastasis. A mutualistic interaction between tumor cells and the surrounding stromal cells promotes the initiation and progression of tumor, in which S100 protein family plays an important role. Our previous research showed that S100A7 bound to RAGE and activated ERK signaling pathway to enhance invasion and metastasis of cervical cancer cells. Moreover, S100A7 could be secreted into the conditioned media and extracellular S100A7 also enhanced cell migration and invasion. Based on our previous research, we will investigate the function of S100A7 in TME, and further evaluate its potential molecular mechanism in tumor metastasis. These studies will significantly increase our understanding of the molecular mechanism of metastasis in cervical cancer, which will provide theoretical basis for new tumor makers and treatment strategy.