Lv Yongqiang, Wang Chaolian, Liu Ruoyu, Wu Shaoxian, Chen Junjun, Zheng Xiao, Jiang Tianwei, Chen Lujun
Department of Neurosurgery, The Third Affiliated Hospital of Suzhou University, Changzhou, Jiangsu, China.
Department of Tumor Biological Treatment, The Third Affiliated Hospital of Suzhou University, Changzhou, Jiangsu, China.
Cell Death Discov. 2024 Aug 22;10(1):373. doi: 10.1038/s41420-024-02138-5.
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.
核调控在癌症治疗中具有潜力，核孔复合体（NPC）作为细胞核与细胞质之间的关键通道，在调节各种生物学过程和癌症中发挥作用。DNA甲基化是一种由DNA甲基转移酶（DNMTs）介导的表观遗传修饰，影响基因表达和细胞分化，对肿瘤细胞的发生和发展至关重要。胶质瘤是最常见的原发性脑肿瘤，其中胶质母细胞瘤尤其具有侵袭性，其特征为侵袭性、迁移能力以及对传统治疗的抗性，导致预后不良。我们的研究表明，NUP37的表达水平影响胶质瘤细胞的增殖和侵袭，并且DNMT1的过表达可以减轻NUP37缺失所引起的不利影响。这些发现表明，NUP37通过与DNMT1相互作用促进胶质瘤细胞的增殖和侵袭。
