PP09 investigates the origin and the role of lipid droplet accumulation - a novel hallmark of cancer progression - and lipid hydrolysis in cancer. Multi-omics studies of non-small cell lung carcinoma (NSCLC) compared to adjacent healthy tissue revealed increased triacylglycerol, ceramide, and lysophospholipid concentrations and concomitant deactivation of several lipid hydrolases. PP09 will study whether these dysregulated lipid hydrolases affect cancer cell aggressiveness and whether they are linked to the (de)activation of oncogenes, lipid or oxidative stress signaling. Another research focus is the role of ABHD5/CGI-58 as well as PNPLA3 and its I148M variant, responsible for higher risk to non-alcoholic fatty liver disease and fibrosis, on the phenotype of hepatoma cells and their crosstalk with fibrogenic stellate cell activation.
