Apoptosis Background

Apoptosis is a crucial cellular function that can become misregulated in cancers, along with cell growth and proliferation. It can be activated in multiple ways throughout the cell, but is mainly characterized by two pathways: intrinsic and extrinsic. The intrinsic pathway is activated in response to cellular stress, which then affects the mitochondria either by swelling through pores or increasing permeability of the membranes (Kroemer et al. 2007). Second mitochondria-derived activator of caspases (SMAC) proteins are then released into the cytoplasm, which deactivate inhibitor of apoptosis proteins (IAPs), allowing the caspases involved in apoptosis to become active (Fesik and Shi, 2001). The extrinsic pathway of apoptosis is activated in response to external signals, which bind to receptors of the tumor necrosis factor (TNF) families. The binding of these ligands to their receptors can activate caspases and indirectly activate transcription factors involved in the inflammatory response and cell death (Adler 2007).