RGL2 Drives the Metastatic Progression of Colorectal Cancer via Preventing the Protein Degradation of β-Catenin and KRAS

Colorectal cancer (CRC) is one of the most common cancers and results in high mortality worldwide, owing to progression, i.e., metastasis. However, molecular mechanism underlying metastatic evolution CRC remains largely unknown. Here, we find that upregulation Ral Guanine Nucleotide Dissociation Stimulator Like 2 (RGL2) commonly detected primary tumors compared normal tissues significantly associated with a poorer prognosis patients. Moreover, RGL2 expression appeared positively correlate potentials cells. Whereas knockdown dramatically suppresses cells vitro vivo, overexpression poorly reconstitution RGL2-silenced enhanced rescued cellular ability, respectively. Computational simulation using Gene Set Enrichment Analysis program cell-based assays demonstrated causally activity Wnt/β-catenin signaling axis Kirsten ras (KRAS)S, as well progression epithelial-mesenchymal transition (EMT) Importantly, was capable preventing protein degradation β-catenin KRAS These findings suggest acts driver promote also serves poor prognostic biomarker