The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.

Biological characteristics of ATP5A1 and its pathogenic mechanisms in human diseases: advances in clinical translation

ATP5A1 acts as a crucial gene that encodes the core α subunit of the mitochondrial F1-ATPase complex to regulate cellular oxidative phosphorylation (OXPHOS) and maintain energy homeostasis. Consequently, its dysregulation—whether through aberrant expression, genomic alterations, or aberrant post-translational modifications—is hypothesized to be a key potential molecular event contributing to the pathogenesis of malignant tumors, neurodegenerative lesions, and metabolic dysregulation.This review systematically summarizes the molecular structure, biological functions, and regulatory networks of ATP5A1. A comprehensive overview of its expression patterns and pathogenic mechanisms across various diseases, including lung, colorectal, liver, and gastric cancers, as well as non-neoplastic conditions, is provided. Besides, emphasis is placed on the clinical translational potential of ATP5A1 as a diagnostic biomarker and therapeutic target, with recent advances in this area critically evaluated. Furthermore, current challenges and limitations in ATP5A1-related research are discussed, and future directions are proposed to facilitate mechanistic investigations and clinical applications. Collectively, this review establishes a comprehensive theoretical framework for understanding the role of ATP5A1 in disease pathogenesis and supports its potential utility in precision diagnostics and therapeutics.

KAT8-mediated epigenetic modifications: Physiological functions, heterogeneity in disease, and advances in targeted development

This work provides a comprehensive framework that clarifies recent controversies—such as whether H4K16ac primarily governs transcription or replication timing, and which KAT8-containing complex catalyzes, which acetylation mark—and establishes a rationale for future precision-targeting strategies and biomarker development grounded in KAT8 functional heterogeneity.

N-Acetyltransferase 10 (NAT10) at the crossroads of metabolism, immunology, and cancer biology

The emerging role of NAT10-mediated N4-acetylcytidine modification of RNA in bone diseases: Current frontiers and future challenges.

AIMS To review the biosynthesis, regulatory mechanisms, and functional roles of N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) RNA modification in bone and joint diseases, and to evaluate its therapeutic potential. MATERIALS AND METHODS A systematic literature search was conducted using PubMed, Web of Science, and Scopus databases for articles published up to May 2026 addressing NAT10, ac4C RNA modification, and bone diseases including osteoporosis, inflammatory bone loss, osteoarthritis, osteosarcoma, and bone marrow mesenchymal stem cell (BMSC) differentiation. Studies investigating ac4C modification mechanisms, detection methods, and therapeutic interventions were critically reviewed and synthesized. KEY FINDINGS NAT10, the primary known ac4C writer, catalyzes ac4C on rRNA, tRNA, and potentially mRNA, thereby regulating RNA stability and translation efficiency. Accumulating evidence indicates that NAT10-mediated ac4C influences skeletal homeostasis through several distinct routes. It promotes osteogenic differentiation of BMSCs by stabilizing RUNX2 mRNA, drives osteoclastogenesis through Fos/NFATc1 signaling, and modulates inflammation in periodontitis and rheumatoid arthritis. It further promotes osteoarthritis by suppressing chondrogenic programs and fuels osteosarcoma through metabolic reprogramming. Pharmacological NAT10 inhibition with Remodelin shows therapeutic potential in preclinical models, although its specificity remains incompletely characterized. SIGNIFICANCE NAT10-mediated ac4C modification represents an emerging regulatory mechanism in skeletal biology. Accumulating evidence supports its involvement in osteoporosis, inflammatory bone loss, osteoarthritis, and osteosarcoma through effects on RNA stability, translation efficiency, and downstream signaling. Substantial gaps nonetheless remain. In particular, it is still unclear how ac4C on specific transcripts controls bone- and cartilage-cell function, and to what extent these modifications are dynamically regulated across disease states.

RNA-Binding Motif Protein 3 as a Therapeutic and Prognostic Target for Drug Discovery

This comprehensive literature review delves into the multifaceted roles of RNA-binding motif protein 3 (RBM3) in cellular processes, disease pathogenesis, and therapeutic potential. RBM3 has been implicated in shaping cell morphology, synaptic protection in neurodegenerative conditions, and regulating gene expression through binding to specific RNA sequences. In cancer, RBM3 exhibits contrasting effects, influencing cell proliferation, tumorigenic potential, and RNA splicing. Clinical studies suggest RBM3 as a predictive biomarker in chemotherapy response for muscle-invasive bladder cancer. Despite promising therapeutic implications in neuroprotection and cancer, challenges persist in understanding the regulatory mechanisms and clinical behavior of RBM3. Further research is warranted to elucidate the molecular mechanisms underlying RBM3’s diverse functions and its significance as a potential target for personalized medicine in cancer therapy. This review underscores the pivotal role of RBPs, particularly RBM3, in disease progression and highlights the need for continued investigation to harness their therapeutic potential effectively. This review evaluates evidence available through December 2025, with particular emphasis on studies published between 2010 and 2025.

Multidimensional roles of NEDD9 in cancer progression: From molecular regulation to clinical translation.

This review provides a comprehensive and integrative analysis of NEDD9 by systematically linking its structural features, multilayered regulatory mechanisms, diverse biological functions, and clinical relevance within a unified conceptual framework.