Complement activation in non-small cell lung cáncer and its effect on tumor progresión

Abstract

HYPOTHESIS The hypothesis of the present work is that tumor cells express on their surface tumorassociated antigens that have the potential to activate the complement system. At the same time, tumor cells have developed mechanisms that make them resistant to complement cytotoxic effects. The subsequent effects of complement activation on complement-resistant cancer cells play a pivotal role in the development of malignant features, ending in tumor progression. OBJECTIVES 1. To study complement activation by the alternative and classical pathways on non-small cell lung cancer (NSCLC) cells and normal bronchial epithelial cells. 2. To study the expression, at the mRNA and protein levels, of the main complement inhibitory proteins in NSCLC and normal bronchial epithelial cells. 3. To study the role of complement in a syngeneic mouse model of lung cancer, with special interest in tumor-associated characteristics of the microenvironment such as angiogenesis and immunosuppression. 4. To evaluate the tumor-promoting effects of complement on NSCLC cells.