Fig. 8.

The NCL-CYTOR-Sam68 complex activated the NF-κB pathway and acted as a prognostic biomarker. a Expression of P65 and phosphorylated P65 in NCL and Sam68 knockdown RKO and SW620 cells by immunoblotting. b Luciferase promoter reporter assays of NF-κB in NCL and Sam68 knockdown cells. c Expression of P65 and phosphorylated P65 in CYTOR knockdown cells and in CYTOR-overexpressing HCT8 and HCT116 cells by immunoblotting. d Luciferase promoter reporter assays of NF-κB in CYTOR knockdown cells. e ROC curve analysis for the combination of CYTOR, NCL and Sam68 in the TCGA, GSE17536 and GSE17537 databases. f 3D curve assay for the relationship between recurrence and the expression distribution of CYTOR, NCL and Sam68. g Kaplan-Meier plots of overall survival for the combination of CYTOR, NCL and Sam68 in GSE17536 database; group 1 has low expression for all three molecules; group 2 has low expression of CYTOR only; group 3 has high expression of CYTOR only; group 4 has high expression of all three molecules. h Schematic model of the function of CYTOR in CRC progression. CYTOR mediates the interaction of NCL and Sam68 through specific motifs in its EXON1 and activates the NF-κB signaling pathway to promote CRC EMT and metastasis