As collective cell migration is intimately involved in different aspects of metazoan development, molecular mechanisms underlying this process are being explored in a variety of developmental contexts. Border cell (BC) migration during oogenesis has emerged as an excellent genetic model for studying collective cell migration. BCs are of epithelial origin but acquire partial mesenchymal characteristics before migrating as a group towards the oocyte. Here, we report that insulin signaling modulates collective BC movement during oogenesis. Supporting the involvement of Insulin pathway, we demonstrate that compromising Insulin-like Receptor (InR) levels in BCs, inhibits their migration. Furthermore, we show that canonical Insulin signaling pathway components participate in this process. Interestingly, visualization of -depleted BC clusters, using time-lapse imaging, revealed a delay in detachment of BC clusters from the surrounding anterior follicle cells and altered protrusion dynamics. Lastly, based on genetic interactions between , the polarity determinant, and a regulatory subunit of Myosin (), we propose that Insulin signaling likely influences activity to engineer border cell detachment and subsequent movement via Myosin.