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m6A Writer METTL3-Mediated lncRNA LINC01125 Prevents the Malignancy of Papillary Thyroid Cancer

Tianyou He1, Hailiang Xia1, Baojie Chen1

  • 1Department of General Surgery, Wuhan Third Hospital (Tongren Hospital of Wuhan University), Wuhan 430060, Hubei, China.

Critical Reviews in Immunology
|October 12, 2023
PubMed
Abstract

Insights

Methyltransferase-like 3 (METTL3) mediates N6-methyladenosine (m6A) modification of long non-coding RNA LINC01125, inhibiting papillary thyroid cancer (PTC) cell invasion, migration, and proliferation. This axis presents a potential therapeutic target for PTC.

Area of Science:

  • Molecular Oncology
  • Epigenetics
  • RNA Biology

Background:

  • Long non-coding RNA (lncRNA) LINC01125 exhibits anti-tumor properties in various cancers.
  • The role and N6-methyladenosine (m6A) modification mechanism of LINC01125 in papillary thyroid cancer (PTC) tumorigenesis are not well understood.

Purpose of the Study:

  • To elucidate the function of LINC01125 in PTC.
  • To investigate the m6A modification of LINC01125 and its regulatory mechanism in PTC tumorigenesis.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess LINC01125 and METTL3 expression.
  • MeRIP, Pearson correlation, bioinformatics, and RNA stabilization assays to determine LINC01125-METTL3 interactions.
  • Transwell, CCK-8, and colony formation assays to evaluate PTC cell migration, invasion, and proliferation.

Main Results:

  • Reduced expression of LINC01125 and METTL3 was observed in PTC tissues.
  • LINC01125 is a downstream target of METTL3-mediated m6A modification and is stabilized by METTL3.
  • Upregulation of LINC01125 or METTL3 suppressed PTC cell invasion, migration, viability, and colony formation.

Conclusions:

  • METTL3-mediated m6A modification of LINC01125 inhibits PTC cell progression.
  • The LINC01125-m6A-METTL3 axis acts as a tumor suppressor in PTC.
  • This axis represents a potential therapeutic target for PTC treatment.

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