Apoptosis in Cancer - An Update

Abstract

Apoptosis is programmed cell death which is essential for development and survival of living organisms. It is a sequentially regulated suicidal programme where cells activate certain enzymes which dissolute their own nuclear component and various protein component of nucleus and cytoplasm. Disturbance of this regulatory pathway may lead to various diseases like autoimmune diseases, neurodegenerative diseases and cancers. The potential mechanisms of apoptosis and its role in cancer are discussed. The ability of apoptosis to modulate the life or death of a cell is also recognized for its immense therapeutic potential. Understanding the mechanisms from this review will give us better insight to the pathogenesis of various diseases including cancer and will open new horizons to therapeutic approaches.

The DNA Repair Gene ERCC6 rs1917799 Polymorphism is Associated with Gastric Cancer Risk in Chinese

“…Several environmental factors such as H pylori infection and consumption of smoking and alcohol have been identified or suspected to add the risk of cancer (Compare et al, 2010;Sankari et al, 2012). H pylori infection, smoking and drinking may aggravate the burden of DNA repair thereby add additional risk for GC development, especially in subjects with insufficient DNA repairing capacity.…”

Steroidal Saponins from Paris polyphylla Induce Apoptotic Cell Death and Autophagy in A549 Human Lung Cancer Cells

“…Caspases take major and a central role in apoptotic mechanism. There are at least two major mechanisms by which a caspase cascade resulting in the activation of effector caspase-3 may be initiated by the most apical caspase, one involving caspase-8 and the other involving caspase-9 (Sankari et al, 2012).…”

Induction of Indoleamine 2,3-dioxygenase (IDO) Enzymatic Activity Contributes to Interferon-Gamma Induced Apoptosis and Death Receptor 5 Expression in Human Non-small Cell Lung Cancer Cells

“…Active caspase-8 can induce the mitochondrial apoptotic pathway by cleaving Bid, freeing the truncated form to translocate to the mitochondria, which leads to mitochondria damage and activates mitochondrial apoptotic downstream signals, including cytochrome c release into the cytosol (Sankari et al, 2012;Tao et al, 2012). As shown in Figure 3A, IFN-γ treatment could dose independently increases the level of cleaved caspase-8 protein and truncated Bid.…”

“…Mitochondria play an important role in the intrinsic and extrinsic apoptotic death pathways (Sankari et al, 2012;Wang et al, 2014). Loss of mitochondrial membrane potential (Δψm) is an indicator of mitochondrial damage during apoptosis.…”