• Xenopus
• PDGF-B
• neural crest
• GLUD2
• glioma
• Zebrafish

My project aimed at unveiling new molecular aspects involved in glioma progression. Since glutamate homeostasis deregulation seems to play a key role in glioblastoma (GBM) aggressiveness, the first part of the project was designed to deepen the role of the mitochondrial enzyme GLUD2 (glutamate dehydrogenase 2), which resulted differentially expressed between GBM patients with different recurrence-free survival after first surgery. I took advantage of Danio rerio embryos as an in vivo model to figure out GLUD2 possible function in regulating cell proliferation and survival, in order to evaluate its potential involvement in tumor growth.
The second part of the project focused on another distinctive hallmark of gliomas, the infiltrative activity, which makes tumor complete surgical resection almost impossible. Given the urgent need of innovative therapeutic strategies, I tried to unveil new molecular mechanisms responsible of gliomas invasive nature. To this purpose, I investigated the role of PDGF-B in cell migration, since its up-regulation seemed to confer in vivo infiltrating properties on glioma tumor cells, exploiting Xenopus laevis neural crest cells (NCC) for their similarity to metastatic cancer cells. This model gave me the opportunity to achieve the final goal of my research, thus the possibility to discover new molecules involved in cell migration modulated downstream of PDGF-B signaling, paving the way towards the identification of new molecular therapeutic targets.