Abstract
The process of apoptosis is essential for maintaining the physiologic balance between cell death and cell growth. This complex process is executed by two major pathways that participate in activating an executioner mechanism leading to chromatin disintegration and nuclear fragmentation. Dysregulation of these pathways often contributes to cancer development and resistance to cancer therapy. Here, we review the most recent discoveries in apoptosis regulation and possible mechanisms for resensitizing tumor cells to therapy.
Highlights
Apoptosis, an orchestrated event in which cells are programmed to die after receiving specific stimuli, is an important component of cell growth control [1]
Death receptors comprise a subset of the tumor necrosis factor (TNF) receptor superfamily characterized by distinct protein motifs, namely death domains (DD) and death effector domains (DED)
First Apoptotic Signal (FAS) receptor mutations have been described in tumors, such as nasal T/NK lymphomas (50%), testicular germ cell tumors (37.5%), non-small cell lung carcinoma (20.2%), melanoma (6.8%) and squamous cell carcinoma of the skin arising from burn scars (14%), among others [33]
Summary
An orchestrated event in which cells are programmed to die after receiving specific stimuli, is an important component of cell growth control [1]. Apoptosis is characterized by morphologic changes, such as chromatin condensation, nuclear fragmentation and reduction of cell volume (known as pyknosis) [2], as well as biochemical changes that include caspase activation, breakdown of DNA and protein and membrane surface modifications that allow the apoptotic cell to be recognized and engulfed by phagocytic cells [3]. An imbalance between life and death of cells can lead to cancer. We review two tightly regulated pathways that converge to produce apoptosis, the mechanisms by which cancer cells evade it and the therapeutic efforts to target these mechanisms in order to induce apoptosis in cancer cells
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