Crosstalk between tumor cells and microenvironment via Wnt pathway in colorectal cancer dissemination

Abstract

Invasion and metastasis are the deadly face of malignant tumors. Considering the high rate of incidence and mortality of colorectal cancer, it is critical to determine the mechanisms of its dissemination. In the parallel investigation of the invasive front and tumor center area of colorectal cancer (CRC), observation of heterogeneous beta-catenin distribution and epithelial-mesenchymal transition (EMT) at the invasive front suggested that there might be a crosstalk between tumor cells and the tumor microenvironment. Wnt signaling pathway is also involved in the cancer progression due to its key role in CRC tumorigenesis. Moreover, in recent years, there is increasing evidence that the regulators of microenvironment, including extracellular matrix, growth factors and inflammatory factors, are associated with the activation of Wnt pathway and the mobility of tumor cells. In this review, we will try to explain how these molecules trigger metastasis via the Wnt pathway.

Figure 1

Schematic illustration of the canonical Wnt/β-catenin signaling pathway. A: In the absence of Wnt ligands, destruction complex phosphylates β-catenin for ubiquitination and proteolytic degradation; B: In the presence of Wnt ligands, formation of destruction complex is not accomplished, resulting in nuclear translocation of β-catenin.