结直肠癌是消化道常见的恶性肿瘤之一，其发病率及死亡率逐年上升。侵袭转移是影响结直肠癌预后的重要因素。目前关于肿瘤微环境中细胞外基质重构与侵袭转移的关系已成为研究热点。我们前期研究发现：结直肠癌中，下调CDX2表达可以促进MMP1的表达，引发以Collagen-Ⅰ为主的细胞外基质重构；另一方面，重构后的Collagen-Ⅰ通过相关细胞信号通路下调CDX2表达。因此，我们推测：结直肠癌中CDX2/MMP1/Collagen-Ⅰ正反馈通路持续激活，可能通过细胞外基质重构促进结直肠癌侵袭转移。基于此，我们将从临床病理、体外细胞、动物模型三个层次，采用临床数据分析、基因芯片、细胞行为学、分子生物学、裸鼠皮下移植瘤及肝脏转移瘤模型技术，探究CDX2/MMP1/Collagen-Ⅰ正反馈通路在结直肠癌侵袭转移中的作用，从新的角度阐明结直肠癌侵袭转移的分子机制并提供潜在治疗靶点。

Colorectal cancer is one of the most common cancer of digestive tract, with its incidence and mortality increasing year by year. Invasion and metastasis is the important factors affecting the prognosis of colorectal cancer. At present, the relationship between extracellular matrix remodeling in tumor microenvironment and invasion and metastasis of malignant tumor has become a research hotspot. Our previous study found that in colorectal cancer, down-regulation of CDX2 expression promoted MMP1 expression, triggering Collagen-Ⅰ-based extracellular matrix remodeling; on the other hand, aligned Collagen-Ⅰdown-regulated CDX2 expression through the signalling pathway. Therefore, we speculate that the persistent activation of CDX2/MMP1/Collagen-Ⅰ positive feedback loop promotes invasion and metastasis of colorectal cancer by extracellular matrix remodeling. Based on this, we will explore CDX2/MMP1/Collagen-Ⅰpositive feedback loop on invasion and metastasis of colorectal cancer by using clinical data analysis, gene chips, cell biology, molecular biology, xenograft and metastatic tumor nude mice models on three levels of clinical pathology, in vitro and animal models, in order to elucidate the molecular mechanism of invasion and metastasis in colorectal cancer from a new perspective and provide potential therapeutic targets.