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解析特异性蛋白1在胶质瘤中的作用:病理生理学及临床意义

Unraveling the role of specificity protein 1 in gliomas: pathophysiology and clinical implications.

作者信息

Naseri Aida, Razi Sepideh, Rezaei Nima

机构信息

Cancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Tehran, Iran.

Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Clin Transl Oncol. 2025 Sep 19. doi: 10.1007/s12094-025-04058-x.

DOI:10.1007/s12094-025-04058-x
PMID:40973878
Abstract

Gliomas present a significant challenge to modern medicine as some of the most diverse and malignant brain tumors. Despite considerable developments in curative measures, the prognosis remains unsatisfactory. A prime reason is that much is obscured about the genetic regulation of glioma pathogenesis. In recent years, specificity protein 1 (Sp1) has been recognized as a central transcription factor that promotes gliomagenesis. Sp1, which is overexpressed in glioma tissues, modulates gene transcription by targeting GC boxes through its zinc finger motifs. As a result, it can influence tumor formation, proliferation, invasion, and distant migration. The present review summarizes the structure, function, and regulation of Sp1. Furthermore, this study elucidates the underlying mechanism by which Sp1 interacts with signaling pathways to fuel tumor growth and chemoresistance. Finally, the current state of Sp1's clinical implications is outlined. These findings reveal the potential benefits of Sp1 as a therapeutic target and diagnostic tool, laying the foundation for future studies.

摘要

神经胶质瘤作为一些最多样化和最恶性的脑肿瘤,对现代医学构成了重大挑战。尽管在治疗措施方面取得了相当大的进展,但预后仍然不尽人意。一个主要原因是,关于神经胶质瘤发病机制的基因调控仍有很多不明确之处。近年来,特异性蛋白1(Sp1)已被公认为促进神经胶质瘤发生的核心转录因子。Sp1在神经胶质瘤组织中过度表达,通过其锌指基序靶向GC盒来调节基因转录。因此,它可以影响肿瘤的形成、增殖、侵袭和远处转移。本综述总结了Sp1的结构、功能和调控。此外,本研究阐明了Sp1与信号通路相互作用以促进肿瘤生长和化疗耐药性的潜在机制。最后,概述了Sp1临床意义的现状。这些发现揭示了Sp1作为治疗靶点和诊断工具的潜在益处,为未来的研究奠定了基础。

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本文引用的文献

1
Mithramycin and its analogs: Molecular features and antitumor action.丝裂霉素及其类似物:分子特征与抗肿瘤作用。
Pharmacol Ther. 2024 Aug;260:108672. doi: 10.1016/j.pharmthera.2024.108672. Epub 2024 Jun 3.
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Glioma.胶质瘤。
Nat Rev Dis Primers. 2024 May 9;10(1):33. doi: 10.1038/s41572-024-00516-y.
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EPIC-0628 abrogates HOTAIR/EZH2 interaction and enhances the temozolomide efficacy via promoting ATF3 expression and inhibiting DNA damage repair in glioblastoma.EPIC-0628 通过促进 ATF3 表达和抑制胶质母细胞瘤中的 DNA 损伤修复,阻断 HOTAIR/EZH2 相互作用,增强替莫唑胺的疗效。
Cancer Lett. 2024 Apr 28;588:216812. doi: 10.1016/j.canlet.2024.216812. Epub 2024 Mar 13.
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Zearalenone Induces Blood-Testis Barrier Damage through Endoplasmic Reticulum Stress-Mediated Paraptosis of Sertoli Cells in Goats.玉米赤霉烯酮通过内质网应激介导的山羊支持细胞副凋亡诱导血睾屏障损伤。
Int J Mol Sci. 2023 Dec 31;25(1):553. doi: 10.3390/ijms25010553.
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Neovascularization directed by CAVIN1/CCBE1/VEGFC confers TMZ-resistance in glioblastoma.CAVIN1/CCBE1/VEGFC 导向的新血管生成赋予胶质母细胞瘤 TMZ 耐药性。
Cancer Lett. 2024 Feb 1;582:216593. doi: 10.1016/j.canlet.2023.216593. Epub 2023 Dec 12.
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as a promising biological control agents for plant pathogens.作为用于植物病原体的有前景的生物防治剂。
Front Microbiol. 2023 Nov 14;14:1285543. doi: 10.3389/fmicb.2023.1285543. eCollection 2023.
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TRIM56 acts through the IQGAP1-CDC42 signaling axis to promote glioma cell migration and invasion.TRIM56 通过 IQGAP1-CDC42 信号轴促进神经胶质瘤细胞迁移和侵袭。
Cell Death Dis. 2023 Mar 4;14(3):178. doi: 10.1038/s41419-023-05702-6.
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Liquid biomarkers in glioma.脑胶质瘤的液体生物标志物。
Brain Tumor Pathol. 2023 Apr;40(2):66-77. doi: 10.1007/s10014-023-00452-x. Epub 2023 Feb 17.
9
LncRNA WEE2-AS1 is a diagnostic biomarker that predicts poor prognoses in patients with glioma.LncRNA WEE2-AS1 是一种诊断生物标志物,可预测胶质瘤患者的预后不良。
BMC Cancer. 2023 Feb 6;23(1):120. doi: 10.1186/s12885-023-10594-y.
10
Therapy with oncolytic viruses: progress and challenges.溶瘤病毒疗法:进展与挑战。
Nat Rev Clin Oncol. 2023 Mar;20(3):160-177. doi: 10.1038/s41571-022-00719-w. Epub 2023 Jan 11.