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METTL3 Promotes OSCC Progression by Down-Regulating WEE1 in a m6A-YTHDF2-Dependent Manner.

Yongxu Su1, Yanjia Hu2, Binbin Qu3

  • 1Department of Oral and Maxilofacial Sugery, Changsha Stomatological Hospital, Changsha, 410004, Hunan, China. suyongxu@zsskqyy1.wecom.work.

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Summary

The study found that METTL3 promotes oral squamous cell carcinoma (OSCC) by reducing WEE1 levels. Inhibiting METTL3 or increasing WEE1 suppressed OSCC progression, offering potential therapeutic targets.

Keywords:
METTL3OSCCWEE1YTHDF2m6A

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Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Oral squamous cell carcinoma (OSCC) is a significant cause of cancer-related deaths.
  • The role of RNA methylation in OSCC progression requires further elucidation.
  • METTL3 is implicated in various cancers, but its specific mechanisms in OSCC are not fully understood.

Purpose of the Study:

  • To confirm the role of METTL3 in promoting OSCC.
  • To investigate the underlying molecular mechanisms of METTL3 in OSCC.
  • To explore the relationship between METTL3, YTHDF2, and WEE1 in OSCC.

Main Methods:

  • Expression analysis of METTL3, YTHDF2, and WEE1 in OSCC cells and tissues.
  • Functional assays (proliferation, invasion, migration, apoptosis) after WEE1 overexpression.
  • MeRIP-qPCR to detect WEE1 m6A levels.
  • Knockdown experiments for METTL3/YTHDF2 to assess WEE1 levels and mRNA stability.
  • In vivo studies using a nude mouse model of OSCC.
  • Immunohistochemistry for Ki-67 and WEE1 expression.

Main Results:

  • METTL3 and YTHDF2 were upregulated, while WEE1 was downregulated in OSCC cells.
  • WEE1 overexpression inhibited OSCC cell proliferation, invasion, and migration, and promoted apoptosis.
  • METTL3 and YTHDF2 bind to WEE1 mRNA, leading to its downregulation and reduced stability.
  • METTL3 inhibition decreased WEE1 m6A levels and weakened YTHDF2-WEE1 interaction.
  • In vivo, WEE1 overexpression suppressed OSCC development, an effect reversed by YTHDF2 overexpression.

Conclusions:

  • METTL3 promotes OSCC progression via the m6A-YTHDF2 pathway, which downregulates WEE1.
  • WEE1 acts as a tumor suppressor in OSCC.
  • Targeting the METTL3/YTHDF2/WEE1 axis may offer a novel therapeutic strategy for OSCC.