Thyroid carcinoma (TC) represents the most prevalent malignancy of the endocrine system. Protein arginine methyltransferase 1 (PRMT1) is a critical member of the protein arginine methyltransferase family in mammals and is involved in multiple biological processes. This study aimed to investigate the function of PRMT1 in TC. In the present study, human TC cell lines (8505C, CAL62, and BCPAP) and a normal human thyroid cell line Nthy‑ori 3‑1 were employed. Small interfering RNA targeting PRMT1 was used to knock down PRMT1 expression in 8505C cells, and PRMT1 overexpression plasmids were transfected into BCPAP cells. Cell viability was assessed using a CCK‑8 and colony formation assays. Apoptosis was measured using flow cytometry and TUNEL assays. Cell migration was assessed using wound healing and Transwell assays. Reverse transcription‑quantitative PCR was used to determine the mRNA expression levels of PRMT1. Western blotting was used to detect the protein expression levels of PRMT1, E‑cadherin, vimentin, H4R3me2as, and zinc‑finger E homeobox‑binding 1 (ZEB1). Notably, PRMT1 expression was elevated in TC (P<0.01). PRMT1 knockdown inhibited TC cell proliferation and migration and concurrently enhanced migration. Furthermore, PRMT1 knockdown suppressed tumor growth and metastasis in a mouse model of TC. PRMT1 downregulation increased E‑cadherin expression and decreased the expression of vimentin, H4R3me2as, and ZEB1 in the TC cells and the mouse model of TC. Conversely, PRMT1 overexpression had the opposite effect on TC malignant characteristics (P<0.05). These findings suggest that PRMT1 knockdown inhibited TC malignancy by downregulating H4R3me2as/ZEB1, thereby highlighting novel therapeutic targets and diagnostic markers for the management of TC.

中文翻译：

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PRMT1 通过上调甲状腺癌中的 ZEB1/H4R3me2as 来加速细胞增殖、迁移和肿瘤生长。

甲状腺癌（TC）代表内分泌系统最常见的恶性肿瘤。蛋白质精氨酸甲基转移酶 1 (PRMT1) 是哺乳动物蛋白质精氨酸甲基转移酶家族的重要成员，参与多种生物过程。本研究旨在探讨PRMT1在TC中的功能。在本研究中，使用了人类 TC 细胞系（8505C、CAL62 和 BCPAP）和正常人类甲状腺细胞系 Nthy-ori 3-1。使用靶向PRMT1的小干扰RNA敲低8505C细胞中PRMT1的表达，并将PRMT1过表达质粒转染至BCPAP细胞中。使用 CCK-8 和集落形成测定评估细胞活力。使用流式细胞术和TUNEL测定法测量细胞凋亡。使用伤口愈合和 Transwell 测定来评估细胞迁移。使用逆转录定量PCR来测定PRMT1的mRNA表达水平。采用Western blotting检测PRMT1、E-钙粘蛋白、波形蛋白、H4R3me2as和锌指E同源盒结合1（ZEB1）的蛋白表达水平。值得注意的是，PRMT1 表达在 TC 中升高（P<0.01）。PRMT1 敲低抑制 TC 细胞增殖和迁移，同时增强迁移。此外，PRMT1 敲低可抑制 TC 小鼠模型中的肿瘤生长和转移。PRMT1 下调会增加 TC 细胞和 TC 小鼠模型中 E-cadherin 的表达，并降低波形蛋白、H4R3me2as 和 ZEB1 的表达。相反，PRMT1过表达对TC恶性特征有相反的影响（P<0.05）。这些发现表明，PRMT1 敲低通过下调 H4R3me2as/ZEB1 抑制 TC 恶性肿瘤，从而突出了用于 TC 管理的新治疗靶点和诊断标记物。