The RET and TRKA pathways collaborate to regulate neuroblastoma differentiation.
作者： Suzanne Peterson , Emil Bogenmann
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摘要: Neuroblastoma (NB) is a childhood cancer that arises in the adrenal gland and often shows differentiated neuronal glial elements. The RET receptor signal pathway functional most NB, while loss of nerve growth factor (NGF) (trkA) gene expression correlates with an aggressive phenotype. Thus, we hypothesized TRKA pathways collaborate to instruct NB differentiation, reminiscent normal maturation. Here, demonstrate activation by cell line-derived neurotrophic (GDNF) increases complex panel malignant human lines, indicative positive feedback mechanism. GDNF also induces cessation concomitant arrest cells G0/G1 phase cycle. Furthermore, synergizes ciliary (CNTF) enhance expression, thereby strengthening NGF-mediated differentiation signal. Differentiated downregulate amplified N-myc gene, concurrent proliferation, expressing neuron-specific markers (i.e., SCG10). Interestingly, maintenance culture independent trophic activity GDNF, but depends on signaling, re-enacting sympathoadrenal (SA) progenitor cells.
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