Connecting the SASP, Innate Immune Signalling, and Lipid Metabolism in Oncogene-Induced Senescence
Juan Carlos Acosta Cobacho
IBBTEC , Santander
Cellular senescence is a stress response that prevents the proliferation of damaged or mutated cells. It is defined by stable cell-cycle arrest and the induction of a complex pro-inflammatory program known as the senescence-associated secretory phenotype (SASP). Oncogene-induced senescence (OIS) serves as a powerful tumour-suppressive mechanism, blocking malignant transformation. However, the persistence of senescent cells, arising from oncogenic activation, anti-cancer therapies, or ageing, can paradoxically promote tumour progression through chronic SASP activity. As advances in therapy extend patient survival, new strategies to identify novel mechanisms to target the beneficial or detrimental impact of cellular senescence in cancer are increasingly urgent.
In my seminar, I will present our recent findings on how innate immune signalling shapes OIS and contributes to tumour suppression in lung adenocarcinoma and highlight our latest results uncovering a lipid biosynthesis pathway that regulates senescence and drives the pro-tumorigenic effects of senescent cancer cells