FOXD1 predicts prognosis of colorectal cancer patients and promotes colorectal cancer progression via the ERK 1/2 pathway

Previous studies indicated a critical role of foxhead box D1 (FOXD1) in human cancers. However, its expression pattern in colorectal cancer (CRC) and the molecular mechanism of FOXD1 on cancer progression remain unknown. In this study, we found that FOXD1 was aberrantly overexpressed in human CRC tissues, and FOXD1 levels were correlated with tumor size, differentiation, TNM stage and lymph node metastasis and poor prognosis. Knockdown of FOXD1 attenuated CRC cell proliferation, migration and invasion. Overexpression of FOXD1 produced the opposite effects. These effects were mediated by activation of the ERK 1/2 signaling pathway, and inhibition of this pathway with a specific ERK 1/2 inhibitor (U0126) could impair the tumor-promoting effects induced by overexpression of FOXD1. Taken together, these findings indicate that FOXD1 promotes tumorgenesis and progression of CRC by activating ERK 1/2 signaling pathway and may represent a potential clinical target.