CEP57L1 and colorectal cancer: Indeed, in our study, using CA induced by pathophysiological factors in diabetes as an experimental model, we demonstrate that AGEs promote CA in colorectal cancer cells, which in turn enhances EMT, migration, and invasion in vitro, and favors metastasis in vivo, with a clearly delineated molecular mechanism of the AGE–KLF5–CEP57L1 axis (Fig. 9).