NUP37 通过 DNMT1 介导的甲基化促进胶质瘤细胞的增殖和侵袭。

IF 6.1 2区生物学 Q1 CELL BIOLOGY

Cell Death Discovery Pub Date : 2024-08-22 DOI:10.1038/s41420-024-02138-5

Yongqiang Lv, Chaolian Wang, Ruoyu Liu, Shaoxian Wu, Junjun Chen, Xiao Zheng, Tianwei Jiang, Lujun Chen

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引用次数: 0

摘要

核调节在癌症治疗中具有潜力，核孔复合体（NPC）是细胞核和细胞质之间的重要通道，在调节各种生物过程和癌症中发挥作用。DNA 甲基化是由 DNA 甲基转移酶（DNMTs）介导的一种表观遗传修饰，影响基因表达和细胞分化，对肿瘤细胞的发展和恶化至关重要。胶质瘤是最常见的原发性脑肿瘤，其中胶质母细胞瘤的侵袭性特别强，具有侵袭性、迁移能力和对常规治疗的耐受性，导致预后不良。我们的研究发现，NUP37的表达水平会影响胶质瘤细胞的增殖和侵袭，而DNMT1的过表达可以缓解NUP37缺失造成的不良影响。这些发现表明，NUP37通过与DNMT1的相互作用促进胶质瘤细胞的增殖和侵袭。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

NUP37 promotes the proliferation and invasion of glioma cells through DNMT1-mediated methylation.

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NUP37 promotes the proliferation and invasion of glioma cells through DNMT1-mediated methylation.

Nuclear regulation has potential in cancer therapy, with the nuclear pore complex (NPC) serving as a critical channel between the nucleus and cytoplasm, playing a role in regulating various biological processes and cancer. DNA methylation, an epigenetic modification mediated by DNA methyltransferases (DNMTs), influences gene expression and cell differentiation, and is crucial for the development and progression of tumor cells. Gliomas are the most common primary brain tumors, with glioblastoma being particularly aggressive, characterized by invasiveness, migration capability, and resistance to conventional treatments, resulting in poor prognosis. Our study revealed that the expression level of NUP37 affects the proliferation and invasion of glioma cells, and that the overexpression of DNMT1 can alleviate the adverse effects caused by NUP37 depletion. These findings suggest that NUP37 promotes the proliferation and invasion of glioma cells through its interaction with DNMT1.

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来源期刊

Cell Death Discovery Biochemistry, Genetics and Molecular Biology-Cell Biology

CiteScore

8.30

自引率

1.40%

发文量

468

审稿时长

9 weeks

期刊介绍： Cell Death Discovery is a multidisciplinary, international, online-only, open access journal, dedicated to publishing research at the intersection of medicine with biochemistry, pharmacology, immunology, cell biology and cell death, provided it is scientifically sound. The unrestricted access to research findings in Cell Death Discovery will foster a dynamic and highly productive dialogue between basic scientists and clinicians, as well as researchers in industry with a focus on cancer, neurobiology and inflammation research. As an official journal of the Cell Death Differentiation Association (ADMC), Cell Death Discovery will build upon the success of Cell Death & Differentiation and Cell Death & Disease in publishing important peer-reviewed original research, timely reviews and editorial commentary. Cell Death Discovery is committed to increasing the reproducibility of research. To this end, in conjunction with its sister journals Cell Death & Differentiation and Cell Death & Disease, Cell Death Discovery provides a unique forum for scientists as well as clinicians and members of the pharmaceutical and biotechnical industry. It is committed to the rapid publication of high quality original papers that relate to these subjects, together with topical, usually solicited, reviews, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.