Animal cells undergo a dramatic series of cell shape changes as they pass through mitosis and divide which depend both on remodelling of the contractile actomyosin cortex and on the release of cell-substrate adhesions. Here, I use the adherent, non-transformed human RPE1 cell line as a model system in which to explore the dynamics of these shape changes, and the function of mitotic adhesion remodelling. Although these cells are highly motile, and therefore polarised in interphase, many will pause migration and elongate to become bipolar prior to mitosis. Interestingly, these cells do not round fully, and many will leave long adhesive tails, which are typically bipolar, connected to the underlying substrate which persist throughout mitosis, and guide cell re-spreading following mitotic exit. Further analysis shows that while many proteins are lost from focal adhesion complexes during mitotic rounding, integrin-rich contacts remain in place along these tails as well as defining the tips of retraction fibres. These adhesions are functionally important in RPE1 cells, since these cells fail to divide when removed from the substrate prior to entry into mitosis. The restoration of cell-substrate adhesions at anaphase are sufficient to rescue division in control cells. However, adhesions are required throughout mitosis for division in cells compromised in their ability to construct an actomyosin  ring. Division in these cells depends on re-spreading, since Ect2 RNAi cells fail to divide on small adhesive islands, but successfully divide on larger patterns with the cytoplasmic bridge connecting daughter cells narrowing as they migrate away from one another. Together these results reveal the importance of coupling adhesion remodeling to mitotic progression.