GRPR and neuroblastoma: Under normoxic and CoCl2-induced hypoxic conditions, silencing the gastrin-releasing peptide receptor (GRP-R) caused a decrease in HIF-1α expression, which blocked vascular endothelial growth factor (VEGF) expression and secretion and led to lower PDK4 levels and higher PDP2 mRNA levels, indicating that GRP-R regulates glucose metabolism in neuroblastoma by modulating HIF-1α, PDK4, and PDP2 [126].