RNF26 promote the proliferation and metastasis of colorectal cancer cells via Wnt pathway
Colorectal cancer (CRC) is the third most common malignant tumor in the world. Identification of key genes for prediction and treatment of disease course and prognosis is urgent to reduce morbidity and mortality of CRC patients. Although dysregulated Ring finger protein 26 (RNF26) expression has been detected in several tumors, the potential regulatory effect of RNF26 on CRC remains uncertain. Here we evaluated the expression of CRC using multiple online platforms, and demonstrated that RNF26 upregulation was consistently observed in CRC relative to normal tissues and correlated with unfavorable prognosis. Then, we provide direct evidence that RNF26 acts as a driver of CRC progression by showing that constructed overexpression cell lines. We analyzed the impact of altering RNF26 level on CRC cell viability and metastasis phenotypes in HCT116 and HCT15 modified cell lines. The results showed that RNF26 overexpression promote cell proliferation, migration, and invasion in vitro, and multiple organ distant metastasis in vivo. Moreover, Wnt signaling pathway was common enriched in these modified cell lines. Therefore, we assumed that RNF26 significantly increased CRC proliferation and metastasis through the RNF26/Wnt axis. These data strongly suggest that RNF26 overexpression may be an effective biomarker to monitor and a prospective therapeutic target to treat CRC. Overall design: Four cell types: HCT116_control, HCT116_OV_RNF26, HCT15_control, HCT15_OV_RNF26, with 3 replicates for each cell type.