Abstract
Cancer is a genetic disease characterized by two features: unregulated cell growth and tissue invasion (metastasis). It can be viewed as the result of a succession of genetic changes during which a normal cell is transformed into a malignant one. Evasion of cell death, apoptosis, is one of the essential changes in a cell that cause this malignant transformation. Hence, reduced apoptosis or its resistance plays a vital role in carcinogenesis. The Bcl-2 family of proteins regulates the mitochondrial apoptotic pathway. Disease states arise upon deregulation of the Bcl-2 family of proteins, where cell death is either promoted or evaded; one of the most common tactic cancer cells utilize to promote survival is anti-apoptotic protein overexpression. Specifically, Bcl-2 overexpression has been shown to be a major chemoresistance factor in a number of human cancers, and for this reason, Bcl-2 targeting is a pharmacologic priority in the quest to reactivate cell death for therapeutic benefit in cancer.
Highlights
Cancer is a genetic disease characterized by two main features: unregulated cell growth and tissue invasion/metastasis
second mitochondria-derived activator of caspase (Smac)/DIABLO or Omi/HtrA2 promotes caspase activation by binding to inhibitor of apoptosis proteins (IAPs) which subsequently leads to disruption in the interaction of IAPs with caspase-3 or -9 [15]
When BH3-only proteins directly activate BAX and BAK, they use their BH3 domain to oligomerize and assemble mitochondrial pores that induce mitochondrial outer membrane permeabilization (MOMP) [35]. This MOMP induces the release of mitochondrial intermembrane space proteins such as cytochrome c and second mitochondriaderived activator of caspases (SMAC) into the cytosol
Summary
Cancer is a genetic disease characterized by two main features: unregulated cell growth and tissue invasion/metastasis. The malignant phenotype requires mutations in several genes that regulate cell proliferation, motility, survival, DNA repair, invasion, and angiogenesis. The normal cell has protective mechanisms that can repair any damage occurs during DNA synthesis or in response to environmental mutagens which are usually abnormal in cancer cells. Too much damage to a normal cell activates a suicide pathway to prevent the damage of the organ. Such a pathway is usually altered in cancer cells, leading to the survival of the damaged cells that normally die. The novel phenotypic characteristics include those that facilitate invasion and metastasis [1]
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