Modulation of NF-κB pathway in cancer therapy by sodium butyrate and Isoproterenol.

Nuclear factor kappa B (NF-κB) is a transcriptional factor that regulates inflammation, cell survival, proliferation, and metastasis. In cancer, NF-κB remains persistently activated, contributing to tumor initiation, progression, immune evasion, and therapeutic resistance- making it a viable therapeutic target for intervention. Sodium butyrate (NaB), a short chain fatty acid produced by gut microbiota, is a potent histone deacetylase (HDAC) inhibitor that enhances histone acetylation and alters gene expression. It plays a pivotal role in chromatin remodeling and and reactivating of tumor suppression genes silenced by mutations. Isoproterenol (ISO), a synthetic β-adrenergic receptor agonist, is used in cardiovascular therapy and modulate NF-κB activation. This review highlights the potential of NaB and ISO in inhibiting NF-κB–driven tumor growth and chemoresistance. We also discuss challenges and future directions for integrating biology and bioinformatics to optimize NF-κB-targeted therapies. Our synthesis offers a new perspective on repurposing metabolic and adrenergic modulators for cancer treatment by emphasizing the translational relevance of NF-κB pathway inhibition.