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蛋白精氨酸甲基转移酶5(PRMT5)通过甲基化ΔNp63α促进舌鳞状细胞癌的细胞迁移和转移。

PRMT5 encourages cell migration and metastasis of tongue squamous cell carcinoma through methylating ΔNp63α.

作者信息

Fan Shijie, Li Wen-Juan, Qi Yucheng, Li Zejiao, He Yao-Hui, Luo Xiushuang, Nie Xiaoyun, Wang Jia, Ji Jinqi, Tian Haoran, Cao Yang, Hou Ya, Ji Ning, Xiao Zhi-Xiong Jim, Wang Xiaobo, Liu Wen, Li Chenghua

机构信息

Center of Growth, Metabolism and Aging, Key Laboratory of Bio-Resources and Eco-Environment of Ministry of Education, Southwest Bio-resources R&D Key Laboratory of Sichuan Province, College of Life Sciences, Sichuan University, Chengdu, China.

State Key Laboratory of Cellular Stress Biology, School of Pharmaceutical Sciences, Xiamen University, Xiamen, China.

出版信息

Cell Death Differ. 2025 Sep 6. doi: 10.1038/s41418-025-01575-8.

Abstract

Tongue squamous cell carcinoma (TSCC) is a common oral malignancy prone to metastasis, whose underlying mechanism remains obscure. Here, we report the oncogenic roles of protein arginine methyltransferase 5 (PRMT5) in TSCC via inhibiting transcription factor ΔNp63α. We found that PRMT5 physically interacts with ΔNp63α, resulting in impairment of ΔNp63α-mediated transcriptional regulation. Further investigation revealed that PRMT5 is significantly upregulated in late stages of TSCC and correlated to poor prognosis. On the other hand, inhibition on ΔNp63α contributes to PRMT5-induced migration and metastasis of TSCC cells. Mechanistically, PRMT5 mediates methylation of ΔNp63α at Arg561, which facilitates CDK1-mediated phosphorylation of ΔNp63α and results in weakened DNA binding of this transcription factor. Consequently, ΔNp63α-mediated suppression on cell migration is attenuated in TSCC. Inhibition of PRMT5 efficiently restrain metastasis of TSCC cells in vivo. Our study is helpful to illuminate the molecular mechanism of TSCC metastasis and to provide a new therapeutic strategy for this malignancy.

摘要

舌鳞状细胞癌(TSCC)是一种常见的易于转移的口腔恶性肿瘤,其潜在机制仍不清楚。在此,我们报道了蛋白质精氨酸甲基转移酶5(PRMT5)通过抑制转录因子ΔNp63α在TSCC中的致癌作用。我们发现PRMT5与ΔNp63α发生物理相互作用,导致ΔNp63α介导的转录调控受损。进一步研究表明,PRMT5在TSCC晚期显著上调,且与预后不良相关。另一方面,对ΔNp63α的抑制作用有助于PRMT5诱导的TSCC细胞迁移和转移。机制上,PRMT5介导ΔNp63α在精氨酸561位点的甲基化,这促进了CDK1介导的ΔNp63α磷酸化,并导致该转录因子的DNA结合能力减弱。因此,TSCC中ΔNp63α介导的对细胞迁移的抑制作用减弱。抑制PRMT5可有效抑制TSCC细胞在体内的转移。我们的研究有助于阐明TSCC转移的分子机制,并为这种恶性肿瘤提供一种新的治疗策略。

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