Objective：To investigate the biological functions and molecular regulatory mechanisms of kinesin family member 11 （KIF11）in colorectal cancer（CRC）. Methods：The expression of KIF11 in CRC was examined by qRT - PCR and public databases. Functional assays（CCK - 8，colony formation，EdU，and Transwell）were employed to evaluate KIF11’s roles in CRC progression. Western blot，RIP - qPCR，MeRIP - qPCR，and RNA stability assays were performed to elucidate the molecular mechanism of N6 - methyladenosine（m6A）modification for KIF11. RNA sequencing（RNA - seq）and correlation analysis were used to examine the downstream mechanism of KIF11 regulation. Results：KIF11 was highly expressed in CRC and promoted CRC proliferation and migration. Mechanistically，methyltransferase - like 3（METTL3）/insulin like growth factor 2 mRNA binding protein 2（IGF2BP2） enhanced KIF11 mRNA stability and expression in an m6A-dependent way. Furthermore，by means of the PROM1/PI3K/AKT pathway， KIF11 facilitated the progression of CRC. Conclusion：The m6A modification of KIF11 by METTL3/IGF2BP2 contributes to CRC progression via the PI3K/AKT signaling pathway，highlighting its potential as a prognostic biomarker and therapeutic target.