METTL14 在 HBV-HCC 中诱导 FOXP4 mRNA 的 N6-甲基腺苷修饰

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-10-14 eCollection Date: 2024-01-01 DOI:10.7150/jca.101385
Tian-Tian Wang, Yi-Mei Ji, Qian Zhang, Bo Liang, Ting-Ting Fan, Xin Ye
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引用次数: 0

摘要

慢性乙型肝炎病毒感染是导致肝硬化和癌症的重要原因。我们的研究发现,HBV 感染会导致 Foxp4 mRNA 的 m6A 修饰显著增加,从而增强 mRNA 的稳定性,进而提高 Foxp4 mRNA 的水平。对慢性 HBV 患者活检样本的分析表明,在 Foxp4 mRNA 水平升高的同时,经 m6A 修饰的 Foxp4 mRNA 水平也持续上调。从功能上讲,在实验室环境中发现 Foxp4 能促进肝细胞癌(HCC)细胞的增殖、迁移和侵袭。此外,研究还发现 HBV 基因表达可通过调节 HCC 细胞中 Foxp4 mRNA 的稳定性来激活 PI3K/AKT 通路。这项研究为了解 HBV 感染的基本机制及其对癌症发展的潜在影响提供了宝贵的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
METTL14 Induced N6-Methyladenosine Modification of FOXP4 mRNA in HBV-HCC.

Chronic hepatitis B virus infections are a significant cause of liver cirrhosis and cancer. Our research reveals that HBV infection leads to a marked increase in m6A modification of Foxp4 mRNA, resulting in enhanced stability of the mRNA and a subsequent increase in Foxp4 mRNA levels. Analysis of biopsy samples from chronic HBV patients demonstrated consistent upregulation of m6A-modified Foxp4 mRNA levels alongside increased Foxp4 mRNA levels. Functionally, Foxp4 was found to promote proliferation, migration, and invasion of hepatocellular carcinoma (HCC) cells in laboratory settings. Additionally, HBV gene expression was shown to activate the PI3K/AKT pathway by modulating Foxp4 mRNA stability in HCC cells. This study provides valuable insights into the underlying mechanisms of HBV infection and its potential implications for cancer development.

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CiteScore
7.20
自引率
4.30%
发文量
567
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