Knockdown of HNRNPM inhibits the progression of glioma through inducing ferroptosis.

IF 4.3 3区材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2023-10-01 Epub Date: 2023-12-15 DOI:10.1080/15384101.2023.2286782

Jian Wang, Xiaolin Luo, Dehua Liu

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Abstract

Purpose: Ferroptosis acts as an important regulator in diverse human tumors, including the glioma. This study aimed to screen potential ferroptosis-related genes involved in the progression of glioma.

Materials and methods: Differently expressed genes (DEGs) were screened based on GSE31262 and GSE12657 datasets, and ferroptosis-related genes were separated. Among the important hub genes in the protein-protein interaction networks, HNRNPM was selected as a research target. Following the knockdown of HNRNPM, the viability, migration, and invasion were detected by CCK8, wound healing, and transwell assays, respectively. The role of HNRNPM knockdown was also verified in a xenograft tumor model in mice. Immunohistochemistry detected the expression levels of HNRNPM and Ki67. Moreover, the ferroptosis was evaluated according to the levels of iron, glutathione peroxidase (GSH), and malondialdehyde (MDA), as well as the expression of PTGS2, GPX4, and FTH1.

Results: Total 41 overlapping DEGs relating with ferroptosis and glioma were screened, among which 4 up-regulated hub genes (HNRNPM, HNRNPA3, RUVBL1, and SNRPPF) were determined. The up-regulation of HNRNPM presented a certain predictive value for glioma. In addition, knockdown of HNRNPM inhibited the viability, migration, and invasion of glioma cells in vitro, and also the tumor growth in mice. Notably, knockdown of HNRNPM enhanced the ferroptosis in glioma cells. Furthermore, HNRNPM was positively associated with SMARCA4 in glioma.

Conclusions: Knockdown of HNRNPM inhibits the progression of glioma via inducing ferroptosis. HNRNPM is a promising molecular target for the treatment of glioma via inducing ferroptosis. We provided new insights of glioma progression and potential therapeutic guidance.

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敲低HNRNPM通过诱导铁下垂抑制胶质瘤的进展。

目的:铁下垂在包括胶质瘤在内的多种人类肿瘤中起着重要的调节作用。本研究旨在筛选参与胶质瘤进展的潜在铁沉降相关基因。材料和方法:基于GSE31262和GSE12657数据集筛选不同表达基因(DEGs)，分离铁衰相关基因。在蛋白-蛋白相互作用网络的重要枢纽基因中，HNRNPM被选为研究靶点。在敲除HNRNPM后，分别通过CCK8、伤口愈合和transwell试验检测其活力、迁移和侵袭。HNRNPM敲低的作用也在小鼠异种移植瘤模型中得到证实。免疫组化检测HNRNPM和Ki67的表达水平。此外，根据铁、谷胱甘肽过氧化物酶(GSH)、丙二醛(MDA)水平以及PTGS2、GPX4、FTH1的表达来评估铁下沉。结果:共筛选到与铁上吊和胶质瘤相关的41个重叠deg，其中确定了4个上调中枢基因(HNRNPM、HNRNPA3、RUVBL1、SNRPPF)。HNRNPM的上调对胶质瘤有一定的预测价值。此外，HNRNPM的敲低抑制胶质瘤细胞的体外活力、迁移和侵袭，并抑制小鼠肿瘤的生长。值得注意的是，HNRNPM的下调增强了胶质瘤细胞的铁下垂。此外，HNRNPM在胶质瘤中与SMARCA4呈正相关。结论:敲低HNRNPM通过诱导铁下垂抑制胶质瘤的进展。HNRNPM是通过诱导铁下垂治疗胶质瘤的一个有前景的分子靶点。我们为胶质瘤的进展和潜在的治疗指导提供了新的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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