Glioblastoma is a primary brain tumor that is one of the most aggressive and deadliest malignant diseases. Despite treatment, which includes maximum possible surgical removal and subsequent radiotherapy and chemotherapy with temozolomide, it remains incurable. The rapid invasion of glioblastoma cells into the surrounding brain prevents complete removal of the tumor, leaving cancer cells in the brain after surgery. As a result, tumor recurrence is practically inevitable and on average remission only lasts 7 months. CD155 is a type 1 adhesion transmembrane glycoprotein that is overexpressed on the surface of glioblastoma cells. In healthy cells, it participates in contact inhibition and cell adhesion, but cancer cells use its function for their own benefit, which is manifested in its aggressiveness, which is associated with a poor prognosis. A lot of research is aimed at inhibiting the function of CD155 and thereby improving the treatment outcome. We also had a similar aim, namely we wanted to study the effect of the binding of an antibody against CD155 (IgCD155) on the invasion of glioblastoma cells. We were studying whether we can influence cell invasion by targeting a specific protein on the surface of those cancer cells. Before we did a 3D invasion test of cancer cell spheroids in Matrigel for this purpose, we checked what concentration of the antibody could be used without having a toxic effect on cell viability. The MTT viability assay showed that IgCD155 does not affect cell viability even at higher concentrations. However, the invasion assay showed that IgCD155 did not affect the invasion of a differentiated glioblastoma cell line obtained from a glioblastoma tumor biopsy. This thesis’ results represent the first basis for further investigation of the potential treatment of glioblastoma by targeting the CD155 protein.
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