Learning on the Fly: The Interplay between Caspases and Cancer

Figure 2

Examples of cellular phenomena that contribute to the clonal expansion of tumour cells. (a) Cancerous cells evade apoptosis through the upregulation of prosurvival proteins such as BCL-2, thus facilitating their clonal expansion. (b) The complex phenomenon of cell competition enables the elimination of slow-proliferating cells (purple), if confronted with fast-proliferating Myc-expressing cells (orange). Lightning symbols indicate the lethal effect (skull symbol) of Myc-expressing cells (orange) on surrounding neighbours (b). (c) Caspase activation defects in the Drosophila proneural clusters promote an excess of sensory organ precursor cells. The non-apoptotic activation of the caspase cascade via Drice leads to cleaved Shaggy, thus modulating the number of sensory organ precursors (c). (d) Drawing showing a non-cell autonomous caspase-mediated phenomenon that facilitates tumorigenesis. Following ablation of cells though irradiation (red lightning symbol) most of cells die (d). If apoptosis is impeded in such a scenario, by ectopic expression of P35, the so-called undead cells (in orange) release pro-proliferative signals (black arrows) into surrounding neighbours (in green), thus instigating tumour formation (d). The dashed line separates examples in which caspases have cell autonomous versus non-cell autonomous effects.