E2F1 is well known as an oncogene for its role in controlling cell proliferation. However, this transcription factor is also involved in contrasting roles such as apoptosis, DNA repair and cell differentiation. Furthermore, E2F1 is associated with numerous different pathways of metabolism including insulin secretion, glycolysis and oxidative metabolism for example. But interactions between E2F1 and the glutamine metabolism have not been studied so far. Glutamine metabolism is increased in a large majority of cancers. This non-essential amino acid is a source of carbon and nitrogen for biosynthesis, energetics and cellular homeostasis and a large majority of cancers depend on it for survival and growth. Previous results from the lab showed that the transcription of glutamine metabolic genes appears to be strongly increased in E2F1 depleted cells. Since E2F1 has been recognized as an oncogene so far, these results contradict what would be expected in terms of glutamine metabolism. There might be a protective role for E2F1 as an inhibitor of glutamine metabolism and therefore a potential role as a tumor suppressor from this perspective. In this master thesis, we want to demonstrate that the same is true for the RNA translation of these genes. Western blots were performed to test several glutamine metabolic genes protein levels in E2f1-wt and E2f1-ko cells.