Preclinical evidence suggests that KIF23 is a molecule with significant translational potential, demonstrating promising prospects in disease diagnosis, prognostic assessment, and targeted therapy, and further in-depth research on KIF23 will significantly advance precision medicine.
Abstract
Kinesin family member 23 (KIF23), a key regulator of cell division, has attracted growing interest owing to its aberrant expression and functional dysregulation in numerous human diseases. However, its systematic mechanisms of action across various pathological types and its potential for clinical translation remain to be fully elucidated. This review integrates multidisciplinary literature and bioinformatics data to systematically summarize the molecular characteristics, regulatory networks, and core functions of KIF23 in various diseases. Accumulating evidence indicates that KIF23 is overexpressed in numerous malignant tumors, where it drives tumor proliferation, metastasis, and drug resistance by regulating cell cycle progression, the DNA damage response, metabolic reprogramming, and remodeling of the immune microenvironment. Its overexpression is strongly associated with poor prognoses. KIF23 also plays a significant role in various non-cancerous diseases, such as congenital dyserythropoietic anemia, pulmonary arterial hypertension, and neurocognitive disorders. Notably, it exhibits tumor-suppressive effects in specific contexts, including cervical cancer, highlighting its context-dependent function. Preclinical evidence indicates that targeting KIF23 effectively suppresses tumor progression and reverses drug resistance. In conclusion, preclinical evidence suggests that KIF23 is a molecule with significant translational potential, demonstrating promising prospects in disease diagnosis, prognostic assessment, and targeted therapy. Further in-depth research on KIF23 will significantly advance precision medicine.
Emerging evidence has expanded the functional repertoire of SKP2 beyond cell cycle control to encompass metabolism, DNA repair, stemness, tumor microenvironment and immunotherapy response, positioning it as an increasingly attractive target for intervention.
Sheng-An Zheng, Cheng Wang, Xiao-Die Yao et al.· Drug Design, Development and...· 0 citations
Bladder cancer is a long‐standing clinical issue, with frequent recurrence and continuously disappointing results in patients, so that therapeutic development is primarily reliant on delineating the original molecular defects. Increasing interest has turned to the Kinesin Superfamily Proteins (KIFs), basic molecular motors that move along microtubule rails, and are now emerging as important key oncogenic derivers in bladder cancer pathogenesis. This review synthesizes available evidence indicating that several KIFs, specifically KIF4A, KIF14, KIF20A, and KIFC1, function as key oncogenic regulators and represent important prognostic biomarkers and therapeutic targets in bladder cancer. When KIF expression or activity is disrupted, it provides mechanical and signaling support for all the cancer hallmarks, facilitating cellular proliferation, invasion, metastasis, and resistance to highly effective cell death. Its oncogenic activity is generally facilitated by the activation of principal signaling pathways. A remarkable proportion of certain KIF isoforms are commonly overexpressed in cancer, and the scale of such overexpression increases with the severity of adverse clinical predictors, such as increasing disease stage, and patient survival worsens. This nuanced molecular image renders KIFs so highly promising targets for therapeutic intervention and prognostic stratification, and initial exploration of kinesin inhibitors is encouraging to abate chemoresistance, aside from optimizing the efficacy of current immunotherapies. Uncovering modalities that exploit the aggressive bladder cancer cell dependence on KIF motor activity is a highly promising path to clinical application.
Usamah Sayed, Noor Mazin Basheer, M. H et al.· Cell Biology International· 0 citations
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.
Shuling Li, Xiao-Mei Liu, Zheng Zhang et al.· International Journal of Mol...· 0 citations
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.
Shu-Yin Yuan, Qi Deng, Hong-Juan Gao et al.· Frontiers in Cell and Develo...· 0 citations
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.
Yu Zhang, Lin Li, Ya Zhang et al.· Pathology, Research and Prac...· 0 citations
Breast cancer continues to present formidable clinical challenges, particularly in triple-negative and endocrine-resistant subtypes where adaptive stress mechanisms drive therapeutic failure. Nuclear protein 1 (NUPR1), an intrinsically disordered protein, has emerged as a non-mutational hub that has been implicated in integrating metabolic, transcriptional, and cell-survival signals associated with malignant progression. This Review examines how NUPR1 transduces mitogenic stimuli into anabolic programs, while orchestrating autophagic flux, lysosomal biogenesis, and ferroptosis evasion to maintain cellular fitness under oncogenic and therapeutic stress. We discuss its causal roles in endocrine and chemoresistance through chromatin-associated cooperation with estrogen receptor α, activation of DNA-damage repair, and cell-cycle checkpoint control, as well as its contributions to metastatic dissemination via extracellular vesicle-mediated niche remodeling and immunosuppressive macrophage polarization. Furthermore, we evaluate emerging therapeutic avenues, from small-molecule inhibitors and single-domain antibody degraders that disrupt NUPR1 nuclear trafficking, to metabolic drug repurposing strategies such as statins that intercept the insulin–NUPR1 axis. Elucidating NUPR1 biology represents a paradigm shift toward targeting dynamic, stress-adaptive dependencies in breast cancer, offering new precision-oncology opportunities.
Bo Xiang, Tao Liu, Duo Xu et al.· Frontiers in Physiology· 0 citations