Research ReportLeptin enhances the invasive ability of glioma stem-like cells depending on leptin receptor expression

- We explored the role of leptin in cells invasion as well as the signaling pathway.
- Coexpression of Ob-R and CD133 was responsible for leptin-mediated invasion.
- Leptin promoted invasion of CD133+ glioma cells through JAK/STAT3 signaling.

Glioma stem-like cells have been demonstrated to have highly invasive activity, which is the major cause of glioma recurrence after therapy. Leptin plays a role in glioma invasion, however, whether and how leptin contributes to the biological properties of glioma stem-like cells, such as invasion, remains to be explored. In the current study, we aimed to explore the role of leptin during glioma stem-like cells invasion as well as the signaling pathway. We found that glioma stem-like cells exhibited high invasive potential, especially in the presence of leptin, Ob-R coexpressed with CD133 in glioma stem-like cells was showed to be responsible for leptin mediated invasion of glioma stem-like cells. Our results indicated that leptin served as a key intermediary linking the accumulation of excess adipokine to the invasion of glioma stem-like cells, which may be a novel therapeutic target for suppressing tumor invasion and recurrence.