Leukemia inhibitory factor (LIF) is a pleiotropic cytokine of the IL-6 superfamily. LIF acts through a cell-surface receptor complex formed by two subunits, the specific LIF receptor (LIFR) and the glycoprotein 130 (gp130). Little is known about LIF involvement in modulating the neuroendocrine circuitry governing the reproductive function and, specifically, the development of GnRH-secreting neurons. In the present study, we evaluated the effect of LIF on the in vitro migration of GN11 cells, a model of immature and migratory GnRH neurons, and the signalling pathways involved in this process. GN11 cells expressed both LIFR and gp130 subunits. Exposure of GN11 cells to 100 ng/mL LIF resulted in activation of the Janus kinases (Jaks)/ signal transducer and activator of transcription 3 (STAT3), MAPK/ERK1/2 and phosphatidylinositol 3-kinase (PI3-K)/protein kinase B (PKB/Akt) pathways. The selective inhibition of Jaks, MEK (mitogen-activated protein kinase kinase) and PI3-K indicated that these signalling pathways were activated independently by LIF and that Jak2 is not the main kinase involved in LIF signalling. Exposure of GN11 cells to LIF for 3 h induced a concentration-dependent chemotactic response, with a plateau at 100 ng/mL LIF. LIF was also found to induce chemokinesis of GN11 cells. Furthermore, LIF-promoted GN11 migration was the result of the partial and independent contribution of all the three signalling pathways activated by LIF. The present data, together with the observation that LIF and LIFR are expressed prenatally in the mouse nasal compartment, would suggest that LIF may participate in the migration of GnRH neurons.