Controlling secretion to limit chemoresistance

Abstract

The tumor microenvironment influences cancer progression and therapy outcome by mechanisms not yet fully understood. In this issue, Bent et al. (2016) show how chemotherapy causes endothelial senescence. Interestingly, senescent endothelial cells do not mount a typical senescence-associated secretory phenotype but instead acutely secrete IL-6, promoting chemoresistance. This study unveils a physiological switch involving PI3K/AKT/mTOR signaling that restrains the senescence secretory responses to limit the detrimental consequences of persistent inflammation.