As shown in Fig. 8B, the proteasome inhibitor MG132, but not the autophagy inhibitor chloroquine (CQ), which abolishes lysosomal protein degradation, led to the accumulation of endogenous NAT10 in CRC cells upon 5-Fu treatment, suggesting that 5-Fu promotes the proteasome-dependent degradation of NAT10 in CRC cells. This evidence concerns the gene NAT10 and colorectal carcinoma.