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Updated: May 5, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

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Published on: November 2, 2018

NF-κB Signaling in Prostate Cancer Progression: Inflammatory Mediators, Survival Pathways, and Regulatory Axes.

Ranyah Al-Hakm^1,2, Alaa Muayad Altaie^1,3, Anania Boghossian¹

¹Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah P.O. Box 27272, United Arab Emirates.

|May 4, 2026

Summary

Prostate cancer progression involves inflammation and immune dysregulation, particularly through nuclear factor kappa B (NF-κB) signaling. This review explores NF-κB

Keywords:

BCL-2 BCL-3 NF-κB signaling apoptosis resistance castration-resistant prostate cancer prostate cancer

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Area of Science:

Oncology
Immunology
Molecular Biology

Background:

Prostate cancer (PC) progression is linked to inflammation and immune dysregulation.
Nuclear factor kappa B (NF-κB) signaling is implicated in PC aggressiveness and treatment resistance.
Mechanisms of NF-κB dysregulation in PC progression are not fully understood.

Purpose of the Study:

To review current evidence on NF-κB signaling in prostate cancer.
To emphasize stage-dependent activation, tumor microenvironment regulation, and downstream effects.
To investigate the potential role of B-cell lymphoma-3 (BCL-3) and its interplay with B-cell lymphoma-2 (BCL-2).

Main Methods:

Synthesis of existing clinical, molecular, and transcriptomic data.
Focus on NF-κB activation patterns across different PC stages.
Analysis of regulatory roles of BCL-3 and BCL-2 in PC.

Main Results:

Constitutive NF-κB activation is observed in multiple PC stages, especially advanced and castration-resistant disease.
BCL-2 overexpression is a known factor in PC apoptosis resistance.
Direct evidence linking BCL-3 to BCL-2 regulation in PC is limited, though suggested by other cancers.

Conclusions:

NF-κB signaling is constitutively active in advanced prostate cancer, contributing to resistance.
The role of BCL-3 as a regulator of NF-κB and BCL-2 in PC is speculative and requires further investigation.
Clarifying the BCL-3/BCL-2 axis is crucial for developing targeted therapies for advanced PC.