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 quantitative real-time PCR (qRT-PCR) techniques and publicSdatabases. CCK8 assay, colony formation assay, EDU assay, and transwell assay demonstrated the function of KIF11 in CRC progression, and Western blot(WB), RIP-qPCR, MeRIP-qPCR, and RNA stability assays elucidated 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: The results indicated that KIF11 was highly expressed in CRC and promoted CRC proliferation and migration. Mechanistically, METTL3/IGF2BP2 affected KIF11 mRNA stability and positively regulated KIF11 expression in an m6A-dependent way. Meanwhile, By means of the PROM1/PI3K/AKT pathway, KIF11 facilitated the progression of CRC. Conclusions: The m6A modification of KIF11 by METTL3/IGF2BP2 contributes to CRC progression via the PI3K/AKT signaling pathway, and it may function as a potential prognostic biomarker and therapeutic target for CRC.