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MEX3A在肿瘤发生中的作用:机制、肿瘤特异性效应及治疗意义(综述)

Role of MEX3A in tumorigenesis: Mechanisms, tumor‑specific effects and therapeutic implications (Review).

作者信息

Tang Lulu, Zhang Li, Yao Shun, Li Xin, Wang Yongfeng, Liu Qian, Li Jiajia, Wen Guorong, An Jiaxing, Jin Hai, Zhu Jiaxing, Tuo Biguang

机构信息

Department of Gastroenterology, Digestive Disease Hospital, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.

出版信息

Int J Mol Med. 2025 Sep;56(3). doi: 10.3892/ijmm.2025.5579. Epub 2025 Jul 11.


DOI:10.3892/ijmm.2025.5579
PMID:40641106
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12270390/
Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b6/12270390/ee80586f8fd2/ijmm-56-03-05579-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b6/12270390/fac5a2246e2b/ijmm-56-03-05579-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b6/12270390/d9e4a93215f8/ijmm-56-03-05579-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b6/12270390/ee80586f8fd2/ijmm-56-03-05579-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b6/12270390/fac5a2246e2b/ijmm-56-03-05579-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b6/12270390/d9e4a93215f8/ijmm-56-03-05579-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63b6/12270390/ee80586f8fd2/ijmm-56-03-05579-g02.jpg

相似文献

[1]
Role of MEX3A in tumorigenesis: Mechanisms, tumor‑specific effects and therapeutic implications (Review).

Int J Mol Med. 2025-9

[2]
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[7]
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[8]
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[10]
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本文引用的文献

[1]
MEX3A promotes cell proliferation by regulating the RORA/β-catenin pathway in hepatocellular carcinoma.

World J Gastrointest Oncol. 2025-4-15

[2]
Innovative Applications of Bacteria and Their Derivatives in Targeted Tumor Therapy.

ACS Nano. 2025-2-11

[3]
Cancer statistics, 2025.

CA Cancer J Clin. 2025

[4]
Digestive cancers: mechanisms, therapeutics and management.

Signal Transduct Target Ther. 2025-1-15

[5]
Recent advances in HPV biotechnology: understanding host-virus interactions and cancer progression - a review.

Int J Surg. 2024-12-1

[6]
Chimeric Antigen Receptor-T Cells in Colorectal Cancer: Pioneering New Avenues in Solid Tumor Immunotherapy.

J Clin Oncol. 2025-3-10

[7]
Anti-PD-1 and anti-PD-L1 antibodies for glioma.

Cochrane Database Syst Rev. 2025-1-8

[8]
Treatment advances across the cervical cancer spectrum.

Nat Rev Clin Oncol. 2025-3

[9]
Corrigendum to "PARP inhibitors in gliomas: Mechanisms of action, current trends and future perspectives" [Cancer Treat. Rev. 131 (2024) 102850].

Cancer Treat Rev. 2025-1

[10]
Splicing dysregulation: hallmark and therapeutic opportunity in pancreatic cancer.

Trends Mol Med. 2024-12-7

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