KIF11, a member of the kinesin family, plays a vital role in the formation and maintenance of the mitotic spindle, thus being crucial for the accurate separation of daughter cells during mitosis [3]. It is also involved in regulating the cell cycle and is associated with many biological processes and diseases. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying its functions.

In photoreceptor cells, KIF11 localizes at the transition zone of the photoreceptor cilium. KIF11 depletion leads to malformations of the ciliary axoneme and membranous discs, resulting in photoreceptor degeneration and drusen-like deposit accumulation in the retina [1]. In hepatocellular carcinoma, knockdown of KIF11 causes cellular senescence and inhibits tumor progression, associated with increased expression of CDKN2A [2]. In endometrial cancer, KIF11 knockdown inhibits cell proliferation, migration, and invasion, and induces G2/M phase arrest and apoptosis [4]. Similar inhibitory effects on cancer cell growth and progression are seen in thyroid cancer, pancreatic ductal adenocarcinoma, non-small cell lung cancer, adrenocortical carcinoma, and childhood acute lymphoblastic leukemia when KIF11 is knocked down or inhibited [5,6,7,8,9].

In conclusion, KIF11 is essential for mitosis and cell cycle regulation. Model-based research, especially KO/CKO mouse models, has revealed its significant roles in maintaining photoreceptor cilium integrity and in the progression of multiple cancers. Understanding KIF11's functions provides potential prognostic biomarkers and therapeutic targets for related diseases.