Deregulated Apoptosis in Female Genital Tract Cancer
نویسنده
چکیده
Apoptosis is initiated via the mitochondrial or the death receptor pathway. Central to the mitochondrial pathway is the release of cytochrome c from the mitochondria, leading to activation of the caspase cascade and execution of apoptosis.1 The mitochondrial pathway is regulated by the BCL-2 family of proteins, i.e. proapoptotic BAX and BAK as well as antiapoptotic BCL-2 and BCL-xL. The death receptor pathway is activated when the cell surface death receptor—Fas—is bound by its ligand—Fas ligand, resulting in recruitment of the adaptor protein FADD and procaspase 8 to the intracellular domain of the death receptor and subsequent caspase activation. Inhibitors of apoptosis have been shown to play a role in oncogenesis through direct caspase and procaspase inhibition (primarily caspases 3 and 7) and transcription factor NF-κB signaling.2 In addition, some proapoptotic molecules are downregulated or inactivated in cancer cells, such as Fas, p53, Bax or Bid.3 Deregulated Apoptosis in Female Genital Tract Cancer
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تاریخ انتشار 2009