Research progress on BTG2 in non-tumor diseases (Review)
TL;DR
This review systematically synthesizes advances in the pivotal, context-dependent roles of BTG2 in non-tumor pathologies, including fibrotic, neurological, cardiovascular, inflammatory, metabolic and other systemic diseases.
Abstract
The B-cell translocation gene 2 (BTG2), originally identified as a tumor suppressor, has been extensively studied in oncology research. However, its multifaceted functions in non-tumor diseases are still being recognized but not entirely understood. This review systematically synthesizes advances in the pivotal, context-dependent roles of BTG2 in non-tumor pathologies, including fibrotic, neurological, cardiovascular, inflammatory, metabolic and other systemic diseases. BTG2 is not merely a binary regulator but a context-sensitive molecular hub. Specific disease microenvironments, cell types and pathological stages contribute to its biological impact, whether protective or pathogenic. For instance, BTG2 promotes protective microglial activation in Alzheimer's disease while exacerbating neuronal death in acute spinal cord injury. Mechanistically, BTG2 influences cell fate decisions involving apoptosis, senescence, inflammation and metabolism by integrating signals from various pathways at the intersection of major regulatory networks, such as the neuro-immune-epigenetic axis and the metabolic-epigenetic-fibrosis network. It has emerged as a promising dual-purpose biomarker for disease diagnosis and prognosis, as well as a potential therapeutic target, owing to its dose-sensitive expression and regulatory position. However, because of its functional duality, therapeutic targeting necessitates precise, context-specific strategies. This review offers a novel, integrative perspective on BTG2 in non-tumor biology, underscoring its implication as a key regulatory node with extensive translational potential.