Apoptosis Dysregulation in Prostate Cancer: The BAX/BCL-2 Dynamics and Caspase Cascade Activation Networks
DOI:
https://doi.org/10.62382/jcbt.v3i3.121Keywords:
Prostate cancer, Apoptosis dysregulation, BAX/BCL-2 ratio, Caspase cascade, Androgen receptor signaling, Therapeutic targetsAbstract
Prostate cancer is one of the most diagnosed cancers in men and a leading cause of cancer-related deaths across the globe. Apoptotic disruption is a hallmark of prostate tumorigenesis that is highly regulated and ensures maintenance of cellular homeostasis. There has been growing evidence that the balance of the B-cell lymphoma 2 (BCL-2) family proteins, especially the ratio between pro-apoptotic BCL-2-associated X protein (BAX) and anti-apoptotic BCL-2, is a leading factor in the control of mitochondrial apoptosis and a contributing factor to prostate cancer progression and resistance to treatment. Under normal prostate conditions, the survival of epithelial cells via intricate stromal epithelial communications is coordinated by the androgen receptor (AR) signaling, and androgen deprivation leads to apoptotic regression of prostate epithelial cells. But at the advanced stage of disease progression, the tumors of the prostate gland often transform into androgen-independent or castration-resistant forms with high BCL-2 expression levels and low apoptosis susceptibility. The mechanisms of apoptosis dysregulation in prostate cancer are presented in this review through the BAX/BCL-2 control of apoptosis, and downstream regulation of the caspase cascade. It also discusses the role of changes in the major signaling pathways involving phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), signal transducer and activator of transcription 3 (STAT3), nuclear factor kappa light chain enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) in the regulation of the activity of BCL-2 and the survival of tumor cells. Besides this, developing regulatory networks between microRNAs and autophagy-related proteins (Beclin-1 and Autophagy/beclin-1 regulator 1 (AMBRA1)) and other regulators are also discussed in terms of their roles in controlling apoptosis and responsiveness to treatment. The existing therapeutic plans of BCL-2 and it signaling partners are also considered, where the potential and shortcomings of the existing inhibitors in the clinical context are outlined. Together, the knowledge of the complex regulation of the apoptotic pathways in prostate cancer offers some valuable information on the development of the disease and the means of resistance. Inhibiting the BAX/BCL-2 axis and caspase-driven apoptotic signaling can thus provide good prospects in the elaboration of more applicable treatment approaches to the treatment of advanced and castration-resistant prostate cancer (CRPC).
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Copyright (c) 2026 Ahmed Hassan Ali, Emily Nguyen, Chinedu Okafor, Eero Nieminen
This work is licensed under a Creative Commons Attribution 4.0 International License.
