IFN signaling as regulator of tumor angiogenesis

Lung cancer is among the most common and deadliest types of cancer worldwide. Non-small cell lung cancer (NSCLC) represents the most prevalent form. For tumor growth, a continuous supply of nutrients and oxygen is required, which is delivered to the tumor tissue through blood vessels. These vessels are composed of specialized tumor endothelial cells (TECs), which, compared to normal endothelial cells, exhibit tumor-promoting properties and influence the immune response. Our research project investigates a specific immune signaling pathway that is activated by type I interferons (IFNs). The goal is to determine how this pathway affects the behavior of TECs in NSCLC. Our initial data show that the IFN-induced gene Interferon alpha inducible protein 27 (IFI27) is particularly active in TECs and may influence tumor growth. To test this hypothesis, we analyze tumor tissue samples from NSCLC patients using state-of-the-art molecular biology techniques. Single-cell sequencing allows us to precisely study the activity of IFI27 and the IFN signaling pathway at the cellular level. The insights gained will then be validated in independent tissue samples from NSCLC patients. Another focus of the project is the functional role of IFI27 in endothelial cells. Using CRISPR/Cas9 technology, we selectively alter gene activity to investigate its effects on cellular behavior, especially angiogenesis. Finally, we will examine the significance of IFI27 in vivo: using a nanoparticle-based system, we will specifically silence the gene in the endothelial cells of a lung cancer mouse model to assess its impact on tumor growth and vascular behavior. This project aims to improve our understanding of the role of TECs in lung cancer with the long-term goal of developing new therapeutic approaches that specifically target tumor-associated blood vessels.

No additional funding sources recorded.