The Role of the BCL2 Family in Targeted Anticancer Response as Apoptotic Mediators

The process known as “programmed cell death,” or apoptosis, is mediated by caspases and regulates tissue homeostasis. There are two pathways by which this process occurs: the intrinsic mechanism, also known as the mitochondrial pathway, and the extrinsic pathway, which is mediated by death receptors. The intrinsic path, which initiates cell death by permeabilizing the mitochondrial membrane and releasing components that induce apoptosis, is regulated by the BCL-2 protein family, which is encoded by the BCL-2 gene. These family proteins' four BCL-2 homology domains (BH1-4) are essential to their operation, and their shared BH domains enable smoother interactions among members of the same family and can also be used as markers of pro- or anti-apoptotic activity. Cell death may be delayed because of BCL-2 overexpression. Several cancers, such as lung, breast, melanoma, and chronic lymphocytic leukemia, as well as Multiple Sclerosis and diabetes, have been linked to changes in BCL-2 expression. This review examines the importance of BCL-2 family interactions for both health and disease, as well as the therapeutic potential to modulate them.