PRMT4 reduced erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells by Nrf2/GPX4 pathway

IF 2.1 4区医学 Q3 TOXICOLOGY Journal of Environmental Pathology Toxicology and Oncology Pub Date : 2024-07-01 DOI:10.1615/jenvironpatholtoxicoloncol.2024053754

Xiaoping Pu, Hong Wu, Xiaoyan Liu, Fang Yang

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Abstract

Nasopharyngeal carcinoma (NPC) is one of the common malignant tumors in clinic. In the current study, we aim to investigate the effects of PRMT4 on erastin-induced ferroptosis in NPC by cisplatin resistant. PRMT4 expression in patients with Nasopharyngeal carcinoma by cisplatin was up-regulated. PRMT4 up-regulation promoted cell growth of erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells. PRMT4 down-regulation reduced cell growth of erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells. PRMT4 promoted Tumor volume in mice model of erastin-induced Nasopharyngeal carcinoma by cisplatin. PRMT4 up-regulation reduced erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells by Mitochondrial damage. PRMT4 up-regulation induced Nrf2 protein expression in model of erastin-induced Nasopharyngeal carcinoma by cisplatin. Nrf2 reduced the effects of si-PRMT4 on cell growth of erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells. Nrf2 inhibitor reduced the effects of PRMT4 on cell growth of erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells. Nrf2 reduced the effects of si-PRMT4 on erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells by Mitochondrial damage. PRMT4 protein interlinked with Nrf2 protein to decrease Nrf2 Ubiquitination. Methylation increased PRMT4 DNA stability. Collectively, our data reveal that PRMT4 reduced erastin-induced ferroptosis in Nasopharyngeal carcinoma cisplatin resistant cells by Nrf2/GPX4 pathway, suggesting that targeting PRMT4 may present as a potential strategy against the develo

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PRMT4 通过 Nrf2/GPX4 通路降低了依拉斯汀诱导的顺铂耐药鼻咽癌细胞的铁蛋白沉积率

鼻咽癌（NPC）是临床上常见的恶性肿瘤之一。本研究旨在探讨 PRMT4 对顺铂耐药的鼻咽癌患者中厄拉斯汀诱导的铁蛋白沉积的影响。PRMT4的上调促进了顺铂耐药鼻咽癌细胞中依拉斯汀诱导的铁蛋白沉积的细胞生长。PRMT4下调会降低依拉斯汀诱导的顺铂耐药鼻咽癌铁中毒细胞的生长。PRMT4 促进了顺铂诱导的依拉斯汀鼻咽癌小鼠模型的肿瘤体积。PRMT4上调可减少依拉斯特诱导的顺铂耐药鼻咽癌细胞线粒体损伤的铁变态反应。上调 PRMT4 可诱导 Nrf2 蛋白在顺铂诱导的厄拉斯汀鼻咽癌模型中的表达。Nrf2能降低si-PRMT4对顺铂耐药鼻咽癌细胞中依拉斯汀诱导的铁突变细胞生长的影响。Nrf2 抑制剂降低了 PRMT4 对顺铂耐药鼻咽癌细胞中麦拉宁诱导的铁蛋白沉积对细胞生长的影响。Nrf2通过线粒体损伤降低了si-PRMT4对依拉斯汀诱导的顺铂耐药鼻咽癌铁中毒的影响。PRMT4 蛋白与 Nrf2 蛋白相互连接，减少了 Nrf2 的泛素化。总之，我们的数据揭示了PRMT4通过Nrf2/GPX4途径减少了厄拉斯汀诱导的顺铂耐药鼻咽癌细胞的铁卟啉沉着，这表明靶向PRMT4可能是一种潜在的抗癌策略。

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来源期刊

Journal of Environmental Pathology Toxicology and Oncology 医学-毒理学

CiteScore

3.80

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： The Journal of Environmental Pathology, Toxicology and Oncology publishes original research and reviews of factors and conditions that affect human and animal carcinogensis. Scientists in various fields of biological research, such as toxicologists, chemists, immunologists, pharmacologists, oncologists, pneumologists, and industrial technologists, will find this journal useful in their research on the interface between the environment, humans, and animals.