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Background <p>To uncover the mechanism of METTL3 and LncRNA DUXAP8 in esophageal squamous cell carcinoma (ESCC) progression.</p> Methods <p>LncRNA DUXAP8 expression was assessed by qRT-PCR. Its overexpression and knockdown in ESCC cells were evaluated for effects on viability and metastasis. WB analyzed PI3K/AKT signaling proteins. MeRIP and RIP assays explored METTL3-DUXAP8 interaction and m6A methylation. In vivo experiments validated the mechanism.</p> Results <p>DUXAP8 was upregulated in ESCC and enhanced cell proliferation, metastasis, and PI3K/AKT activation. It was confirmed that METTL3-DUXAP8 interaction and METTL3 mediated the m6A methylation of DUXAP8. The total level of DUXAP8 and its m6A methylation in TE-1 and KSYE-150 cell lines was decreased significantly by METTL3 knockdown, which inactivated the PI3K/AKT pathway and reduced cell proliferation and metastasis. Xenograft tumor mouse model confirmed that si-METTL3 can reverse DUXAP8-mediated ESCC proliferation via activating the PI3K/AKT pathway.</p> Conclusion <p>METTL3 drives ESCC oncogenesis by binding and positively regulating DUXAP8 in an m6A-dependent manner and activating the PI3K/AKT pathway.</p>

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METTL3-mediated m6A methylation of LncRNA DUXAP8 promoted esophageal squamous cell carcinoma progression by activating the PI3K/AKT signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月5日

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  • Peiyuan Wang,
  • Suyu Chen,
  • Mengxia Lei,
  • Yujie Chen,
  • Hao He,
  • Peng Chen,
  • Weijie Chen,
  • Hang Zhou,
  • Feng Wang,
  • Derong Zhang

摘要

Background

To uncover the mechanism of METTL3 and LncRNA DUXAP8 in esophageal squamous cell carcinoma (ESCC) progression.

Methods

LncRNA DUXAP8 expression was assessed by qRT-PCR. Its overexpression and knockdown in ESCC cells were evaluated for effects on viability and metastasis. WB analyzed PI3K/AKT signaling proteins. MeRIP and RIP assays explored METTL3-DUXAP8 interaction and m6A methylation. In vivo experiments validated the mechanism.

Results

DUXAP8 was upregulated in ESCC and enhanced cell proliferation, metastasis, and PI3K/AKT activation. It was confirmed that METTL3-DUXAP8 interaction and METTL3 mediated the m6A methylation of DUXAP8. The total level of DUXAP8 and its m6A methylation in TE-1 and KSYE-150 cell lines was decreased significantly by METTL3 knockdown, which inactivated the PI3K/AKT pathway and reduced cell proliferation and metastasis. Xenograft tumor mouse model confirmed that si-METTL3 can reverse DUXAP8-mediated ESCC proliferation via activating the PI3K/AKT pathway.

Conclusion

METTL3 drives ESCC oncogenesis by binding and positively regulating DUXAP8 in an m6A-dependent manner and activating the PI3K/AKT pathway.