细胞间调控参与了口腔白斑发生与癌变过程，我们的前期研究提示，炎症因子是口腔白斑癌变中细胞间重要的信息传递分子,白斑中存在多个炎症因子的表达变化，其中CCL18的表达变化最为显著，然而，CCL18在白斑癌变中的作用及与其他炎症因子的关系仍未明确。初步研究结果表明，CCL18可增强口腔癌细胞的迁移运动能力，而运动能力增加是细胞上皮-间质转化（EMT）的重要生物学特征，EMT则是上皮细胞可塑性的主要表现，因此，我们提出以下假设: CCL18参与了口腔白斑癌变过程；CCL18可能影响口腔上皮细胞的可塑性，推动白斑恶性转化细胞突破基底膜发展为浸润癌。为此，本项目拟分析CCL18、受体在口腔白斑癌变中的表达特点；明确CCL18与靶细胞受体结合后对细胞可塑性的影响、所产生的生物学效应，与CXCL12的关系；探究与细胞可塑性相关的调控网络及关键基因。旨在为阐明口腔白斑癌变机制提供新的重要证据和防治新靶点。

Intercellular communication contributes to oral leukoplakia development and carcinogenesis.Our study has confirmed that inflammatory factors are important intercellular messengers in oral leukoplakia carcinogenesis. Many inflammatory factors changed significantly in oral leukoplakia tissues. Among them CCL18 changed most significantly. However, the roles of CCL18 and its associations with other inflammatory factors are still elusive. Our study displayed that CCL18 could promote OSCC cell motility. Cell motility increasing is one important feature in epithelial-mesenchymal transition (EMT). Moreover, EMT is the essential manifestation of epithelial cell plasticity. Then, we hypothesized that CCL18 might be involved in oral leukoplakia carcinogenesis process. CCL18 pathway might regulate cell plasticity and promote the malignant transformed cells to break through basement membrane, leading to invasive carcinoma. Therefore, we set out to investigate the expression characteristics of CCL18 and its receptor. After CCL18 binding to its receptor, the changes of cell phenotype, intercellular signal molecules, and subsequent cell biological behaviors were all examined. The relationship between CCL18 and CXCL12 was also been examined. All those results would be helpful to elucidate the molecular mechanisms of oral leukoplakia carcinogensis, and then provide novel therapeutic target molecules for oral leukoplakia.