

Overexpression of CDX2 suppressed the EMT markers indicating that CDX2 suppresses CRC cell viability, invasion, and metastasis through inhibiting EMT. CDX2 was correlated with expression of EMT markers. Overexpression of CDX2 reduced expression of MMP-2 and diminished cell proliferation, invasion, and migration, while knockdown CDX2 enhanced MMP-2 expression and increased cell proliferation, invasion, and migration in HCT-116 cells. Then, the low expression of CDX2 and high expression of CA199 in combination are positively related with poor prognosis. The levels of CDX2 protein exhibited a positive associated with E-cadherin while negative correlation with N-cadherin. We observed that high expressions of CDX2 and E-cadherin as well as low expressions of N-cadherin were significantly correlated with favorable prognosis. MTT, Western blot, invasion, and migration assays in vitro were employed to explore the function of CDX2. The prognostic value of CDX2 was statistically analyzed. ROC assays were applied to detect cut-off points for IHC scores to distinguish high and low expressions of CDX2 in 46 CRC samples. Expressions of CDX2, E-cadherin, and N-cadherin in all CRC patients were detected by IHC. Forty-six CRC patients were included in the study.

To investigate whether CDX2 is associated with EMT in CRC. However, the role of CDX2 during the activation of EMT in CRC maintains controversial. The epithelial to mesenchymal transition (EMT) is a transdifferentiation process, providing migratory and invasive properties to cancer cells during tumor progression. Studies have confirmed that Caudal Type Homeobox 2 (CDX2) plays a tumor suppressor role in colorectal cancer (CRC) and as a prognostic and predictive marker for colorectal cancer.
