Consistently, the autophagosome-associated form, LC3B-II, was obviously increased in CRC cells upon compound 275# treatment, whereas the level of p62, a specific marker of autophagic flux, was strongly downregulated in a dose-dependent manner (Figure 6B), indicating that autophagy was activated and autophagosomes were formed after treatment. This evidence concerns the gene MAP1LC3B and colorectal carcinoma.