The authors uncover a mechanism for the known antitumor effect exerted by neural precursor cells (NPCs). NPCs migrate into tumors in vivo and secrete endovanilloids, which act as agonists for TRPV1, their receptor expressed by glioma cells. TRPV1 activation causes ER stress and glioma cell death. The reported elevated concentration of TRPV1 in human gliomas and the antitumor effect of synthetic vanilloids suggest that this pathway could be a point of therapeutic intervention and that differential NPC activity, such as that modulated by age, could be a factor influencing brain tumorigenesis.
- Kristin Stock
- Jitender Kumar
- Rainer Glass
