The nucleolus has a significant role in ribosome biogenesis and is an important sensor of stress in the cell. Ribosome biogenesis is necessary to increase protein synthesis capacity during cell growth, cell division and differentiation. It is known that in most malignant tumors, nucleolus has been increased due to the intense ribosome biogenesis which is needed for rapid growth and cell division. As a result of increased ribosome biogenesis, morphological changes in the structure of the nucleus often occur. The effects of numerous anti-inflammatory drugs are achieved by inhibition of ribosomal biogenesis at different steps and inhibition of cell growth thus prevent the growth and division of malignant cells. For a better understanding of the molecular mechanisms by which anti-inflammatory drugs, etoposide and doxorubicin, have an effect on the treatment of malignant tumors in humans, in human A549 cells I tested their influence on the activation of p53 tumor suppressors using the Western blot method. In addition, I tested their effect on the morphological properties of nucleolus by determining expression of UBF and fibrillarin using the immunofluorescence method. Also I tested their influence on the activity of RNA polymerase I and the expression of the messenger RNA for 47S pre-rRNA using the qRT-PCR method. The treatment of cells with etoposide and doxorubicin resulted in activation of p53 tumor suppressor as well as activation of its target gene, p21. Also, treatment with doxorubicin resulted in significant morphological changes in the nucleolus manifested in the formation of fibrillarin and UBF clots at the edges of the damaged nucleolus, while the treatment with etoposide had no effect on the morphological properties of the nucleolus. In addition, doxorubicin prevented the expression of 47S pre-rRNA resulting in inhibition of ribosome biogenesis, while etoposide had no effect on the expression 47S pre-rRNA. Understanding the molecular mechanisms of anti-inflammatory drugs plays an important role in selecting treatment therapy.