Bladder neoplasms and NF-κB: an unfathomed association

Area of Science:

• Oncology
• Molecular Biology
• Immunology

Background:

• Bladder cancer is a prevalent genitourinary malignancy often characterized by recurrence and chemoresistance post-surgery.
• Key risk factors include smoking, aromatic amine exposure, and chronic inflammation.
• Constitutive activation of the transcription factor NF-κB is observed in bladder cancer patients, promoted by inflammatory signals and hypoxia, driving carcinogenesis.

Purpose of the Study:

• To review the role of NF-κB in bladder inflammation, cancer development, and therapeutic resistance.
• To explore how NF-κB orchestrates key molecular interactions and gene expression implicated in bladder cancer progression.

Main Methods:

• Literature review focusing on NF-κB's role in bladder cancer.
• Analysis of NF-κB's interactions with proteins (e.g., PTEN, survivin, VEGF) and regulation of genes (e.g., Trp 53).

Main Results:

• NF-κB activation is linked to bladder cancer progression, recurrence, and resistance to chemotherapy.
• NF-κB influences critical cancer hallmark genes and proteins such as Tp53, PTEN, VEGF, HMGB1, CYLD, USP13, PCNA, BcL-2, JUN, P-gp, twist, and SETD6.
• NF-κB acts as a master regulator in bladder cancer pathogenesis.

Conclusions:

• Further research into NF-κB is crucial for developing effective diagnostic and therapeutic strategies for bladder cancer.
• Targeting NF-κB pathways holds promise for improving treatment efficacy and reducing bladder cancer progression, recurrence, and therapy resistance.