Kinesin family member 11 (KIF11) plays a crucial role in mitosis, particularly in the formation and maintenance of the mitotic spindle. Recent studies have shown that KIF11 is upregulated in various cancers, promoting cancer progression and poor prognosis. This review discusses the mitotic functions of KIF11, including its role in centrosome and spindle events, and its clinical significance. KIF11 is involved in centrosome separation and spindle assembly through interactions with centrosomal proteins and microtubules. It is regulated at the transcriptional, post-transcriptional, and post-translational levels, and its expression is influenced by various factors such as p53, histone modifications, and non-coding RNAs. KIF11 promotes cancer proliferation, invasion, and metastasis by activating signaling pathways like Wnt/β-catenin and mevalonate metabolism. KIF11 inhibitors, including loop 5-binding allosteric inhibitors and competitive ATP-binding inhibitors, have been developed but have shown limited effectiveness due to resistance mechanisms. Future research should focus on understanding the regulatory mechanisms of KIF11 and exploring novel therapeutic strategies to target KIF11 in cancer treatment.Kinesin family member 11 (KIF11) plays a crucial role in mitosis, particularly in the formation and maintenance of the mitotic spindle. Recent studies have shown that KIF11 is upregulated in various cancers, promoting cancer progression and poor prognosis. This review discusses the mitotic functions of KIF11, including its role in centrosome and spindle events, and its clinical significance. KIF11 is involved in centrosome separation and spindle assembly through interactions with centrosomal proteins and microtubules. It is regulated at the transcriptional, post-transcriptional, and post-translational levels, and its expression is influenced by various factors such as p53, histone modifications, and non-coding RNAs. KIF11 promotes cancer proliferation, invasion, and metastasis by activating signaling pathways like Wnt/β-catenin and mevalonate metabolism. KIF11 inhibitors, including loop 5-binding allosteric inhibitors and competitive ATP-binding inhibitors, have been developed but have shown limited effectiveness due to resistance mechanisms. Future research should focus on understanding the regulatory mechanisms of KIF11 and exploring novel therapeutic strategies to target KIF11 in cancer treatment.