Cell migration is required for many biological processes including cancer. The nucleus, being the largest organelle of the cell, can be the limiting factor in the ability of the cell to migrate. To migrate the cytoskeleton rearranges and transmits mechanical signaling to the nucleoskeleton, driving changes in nucleoskeletal composition to control nuclear stiffness. Key components of the nucleoskeleton are Lamin A, Lamin B, and Emerin. More Lamin B results in a softer nucleus, whereas increasing Lamin A and Emerin causes a stiffer nucleus. Increased stiffness of the nucleus restricts its ability to deform and maneuver through small spaces, inhibiting the migration of the cell. While nuclear stiffness regulates 2D single cell migration, little is known of its roles in 3D collective cell migration. To address this unknown, we use border cell migration during Drosophila (fruit fly) oogenesis as our model. My thesis project is focused on how prostaglandins (PGs), short range lipid signaling molecules, regulate the nucleoskeleton to promote on-time border cell migration. PG signaling is a staple characteristic in cancer cells and is associated with aggressive tumors and poorer outcomes for patients. This thesis identifies PG signaling as a regulator of the nucleoskeleton to facilitate migration.  I find that PG signaling restricts Lamin A and Emerin and promotes Lamin B within the border cell cluster. These results suggest that PG signaling softens the nuclei to make it easier for the nuclei to squeeze through small spaces to promote migration. PGs and these nucleoskeleton proteins are found in Drosophila and Humans demonstrating that using Drosophila border cell cluster migration is a great model to understand how PG signaling may be regulating the nucleoskeleton during cancer metastasis.