Abstract
Abstract The sensory cues that developing neurons use to control the pattering of neurite outgrowth are currently not well defined. CXCR4 and the insulin like growth factor receptor (IGF1r) have been implicated in the regulation of chemotaxis, neuronal migration, and axonal guidance. In addition to these chemokine receptors role in the guidance of neuronal development, an increasing body of evidence shows they are up-regulated in many late stage and metastatic cancers. Neuroblastoma, a cancer of neural crest origin, often expresses high levels of CXCR4 and IGF1r, and depending upon the level of differentiation, is capable of producing fully extended axons. The mediator of the cytoskeletal changes seen in axonal extension is primarily carried out by actin polymerization. In order to better understand the role of CXCR4 and IGF1r role in mediating these cytoskeletal changes we used western blots and immunocytochemistry / confocal microscopy to analyze the neuroblastoma cell line SHSY-5Y. We were able to show that indeed both receptors are involved in neuronal outgrowth. However, the individual effects of treatment with the receptors ligand resulted in different cellular morphologies. CXCR4 stimulation resulted in a more differentiated neuronal form, while IGF1r stimulation resulted in a very immature neuronal morphology with shorter broader processes. Finally, we were able to quantitate the effects of treatment to a wide array of phenotypic patterns that shows the connection between our observed morphological changes to show that these observations are real effects of treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1435. doi:10.1158/1538-7445.AM2011-1435
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.