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<p>METTL3‐catalyzed m<sup>6</sup>A methylation drives oncogenic processes in HCC. Foxp4 was recently shown to be overexpressed in HCC, linked to poor prognosis. However, the function of METTL3-Foxp4 axis in HCC is still mainly unknown. Utilizing immunohistochemistry (IHC) and quantitative real-time PCR (qRT-PCR), it was possible to determine Foxp4 expression in HCC tissues and cell lines. In order to evaluate the Foxp4 m<sup>6</sup>A level in HCC, MeRIP-PCR was performed. To find the target gene’s “reader” protein, RNA immunoprecipitation (RIP) was performed. We looked at the biological function and probable mechanism of METTL3-Foxp4 axis in HCC in this study. This study showed that METTL3 increased Foxp4 mRNA levels in HCC in a m<sup>6</sup>A dependent manner, while elevated m<sup>6</sup>A-modified FOXP4 correlates with reduced OS and RFS in HCC patients. Subsequently, METTL3 and YTHDF1 regulated the expression of Foxp4 in HCC cells by affecting the mRNA stability of Foxp4. Functional tests showed that METTL3/Foxp4 axis drives HCC metastasis. In addition, in a large cohort study, Foxp4 expression was linked well with METTL3 and YTHDF1 in HCC. In clinic, a better OS was further observed in HCC patients with low level of “writer”-METTL3, “reader”-YTHDF1 and “target” -Foxp4. Our study reveals a mechanism by which m<sup>6</sup>A-RNA regulates oncogene activity, which might result in the creation of a therapeutic strategy for the treatment of HCC.</p>

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METTL3-mediated m6A modification of FoxP4 promotes HCC metastasis

  • 期刊论文

  • 发表日期：

    2025年8月8日

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  • Guang-zhen Wu,
  • Yi-wei Ren,
  • Yang Liu,
  • Teng Zhao,
  • Zhi-ping Huang,
  • Kai Lu

摘要

METTL3‐catalyzed m6A methylation drives oncogenic processes in HCC. Foxp4 was recently shown to be overexpressed in HCC, linked to poor prognosis. However, the function of METTL3-Foxp4 axis in HCC is still mainly unknown. Utilizing immunohistochemistry (IHC) and quantitative real-time PCR (qRT-PCR), it was possible to determine Foxp4 expression in HCC tissues and cell lines. In order to evaluate the Foxp4 m6A level in HCC, MeRIP-PCR was performed. To find the target gene’s “reader” protein, RNA immunoprecipitation (RIP) was performed. We looked at the biological function and probable mechanism of METTL3-Foxp4 axis in HCC in this study. This study showed that METTL3 increased Foxp4 mRNA levels in HCC in a m6A dependent manner, while elevated m6A-modified FOXP4 correlates with reduced OS and RFS in HCC patients. Subsequently, METTL3 and YTHDF1 regulated the expression of Foxp4 in HCC cells by affecting the mRNA stability of Foxp4. Functional tests showed that METTL3/Foxp4 axis drives HCC metastasis. In addition, in a large cohort study, Foxp4 expression was linked well with METTL3 and YTHDF1 in HCC. In clinic, a better OS was further observed in HCC patients with low level of “writer”-METTL3, “reader”-YTHDF1 and “target” -Foxp4. Our study reveals a mechanism by which m6A-RNA regulates oncogene activity, which might result in the creation of a therapeutic strategy for the treatment of HCC.