Tang Lulu, Zhang Li, Yao Shun, Li Xin, Wang Yongfeng, Liu Qian, Li Jiajia, Wen Guorong, An Jiaxing, Jin Hai, Zhu Jiaxing, Tuo Biguang
Department of Gastroenterology, Digestive Disease Hospital, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
Int J Mol Med. 2025 Sep;56(3). doi: 10.3892/ijmm.2025.5579. Epub 2025 Jul 11.
Muscle excess 3A (MEX3A), a dual‑function RNA‑binding protein with E3 ubiquitin ligase activity, is a pivotal regulator of tumorigenesis. By modulating mRNA stability, translation and targeted protein degradation, MEX3A orchestrates key oncogenic processes, including tumor stemness maintenance, proliferation, migration and immune evasion. MEX3A is aberrantly expressed in various malignancies, such as colorectal and breast cancer, hepatocellular carcinoma and glioblastoma, where it engages key signaling pathways, including the Wnt/β‑catenin, PI3K/AKT and NF‑κB pathways. Mechanistically, MEX3A directly regulates oncogenic and tumor suppressor transcripts, influencing the cell dynamics within the tumor microenvironment. Furthermore, MEX3A upregulation is associated with a poor prognosis and therapy resistance, highlighting its potential as a prognostic biomarker and therapeutic target. The present review aimed to summarize the molecular functions, tumor‑specific roles and translational relevance of MEX3A, bridging the gap between mechanistic insight and clinical applications. Future studies exploring MEX3A‑targeted interventions may reveal novel strategies for precision oncology.
肌肉过量 3A(MEX3A)是一种具有 E3 泛素连接酶活性的双功能 RNA 结合蛋白,是肿瘤发生的关键调节因子。通过调节 mRNA 稳定性、翻译和靶向蛋白降解,MEX3A 协调关键的致癌过程,包括肿瘤干性维持、增殖、迁移和免疫逃逸。MEX3A 在各种恶性肿瘤中异常表达,如结直肠癌、乳腺癌、肝细胞癌和胶质母细胞瘤,在这些肿瘤中它参与关键信号通路,包括 Wnt/β-连环蛋白、PI3K/AKT 和 NF-κB 通路。从机制上讲,MEX3A 直接调节致癌和抑癌转录本,影响肿瘤微环境中的细胞动态。此外,MEX3A 的上调与预后不良和治疗耐药相关,突出了其作为预后生物标志物和治疗靶点的潜力。本综述旨在总结 MEX3A 的分子功能、肿瘤特异性作用和转化相关性,弥合机制见解与临床应用之间的差距。未来探索针对 MEX3A 的干预措施的研究可能会揭示精准肿瘤学的新策略。
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