Menin is the protein mutated in patients with multiple endocrine neoplasia type 1 (MEN1) syndrome and their corresponding sporadic tumor counterparts. Here, we have uncovered a novel function for menin in promoting proper cell division. We show that menin localizes to the mitotic spindle poles and the mitotic spindle during early mitosis and to the intercellular bridge microtubules during cytokinesis in HeLa cells. Menin depletion led to defects in spindle assembly and chromosome congression during early mitosis, lagging chromosomes during anaphase, defective cytokinesis, multinucleated interphase cells, and cell death. Additionally, pharmacological inhibition of the menin-MLL1 interaction also led to similar cell division defects. These results indicate that menin and the menin-MLL1 interaction are important for proper cell division. These results highlight a novel function for menin in cell division and aid our understanding of how mutation and misregulation of menin promotes tumorigenesis.