Fig. 4
From: STK16 promoted colorectal cancer progress in a c-MYC signaling-dependent manner
STK16 Positively Activated c-MYC Signaling via Stabilizing c-MYC. A. GSEA analysis of TCGA database, patients grouped by the expression level of STK16. B. IB assays assessed the expression of c-MYC signaling-related proteins in cancer cells stably expressing sgCtrl or sgSTK16. C. Treated cancer cells with autophagy-lysosome pathway inhibitor (chloroquine, CQ) or ubiquitin-proteasome pathway inhibitor (MG132), and immunoblotting assays assessed the expression of c-MYC in HEK293T cells. D. Transfected his-ubiquitin plasmid into HEK 293T cells, and IB assays assessed the poly-ubiquitination level of c-MYC in HEK293T cells stably expressing vector or STK16. E, F. Transfected his-ubiquitin plasmid into cells, and IB assays assessed the poly-ubiquitination level of c-MYC in HEK293T or RKO cells stably expressing sgCtrl or sgSTK16. G, H. CHX was applied to inhibit endogenous protein synthesis, and IB assays assessed the degradation rate of c-MYC in HEK293T cells ectopically expressing vector, STK16 WT, or STK16 T198A. I. 63 colorectal cancer samples were collected from People’s Hospital of Xinjiang Uygur Autonomous Region. Statistical analysis of the correlation between the expression level of STK16 and the expression level of c-MYC. All IB assays were conducted three times, and consistent results were obtained. Statistical analysis used Student’s t-test