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m6A methyltransferase METTL3 inhibits endometriosis by regulating alternative splicing of MIR17HG

Qian Li1, Li Yang1, Feng Zhang1

  • 1Department of Gynecology, The Third Affiliated Hospital of Zhengzhou University and Henan Province Women and Children's Hospital, Zhengzhou, China.

Reproduction (Cambridge, England)
|November 29, 2022
PubMed

Insights

Methyltransferase like 3 (METTL3) N6-methyladenosine (m6A) modification plays a key role in endometriosis (EMs). METTL3 prevents EMs progression by upregulating MIR17HG expression, impacting cell behavior and hormone levels.

Area of Science:

  • Reproductive biology
  • Molecular oncology
  • Epigenetics

Background:

  • Endometriosis (EMs) involves inflammation and abnormal immune responses.
  • N6-methyladenosine (m6A) modification regulates inflammatory responses.
  • The role of METTL3 in EMs pathogenesis requires further investigation.

Purpose of the Study:

  • To investigate the role of methyltransferase like 3 (METTL3) in endometriosis.
  • To explore the relationship between METTL3, MIR17HG, and EMs progression.
  • To determine the impact of METTL3 on estradiol and lipoprotein levels in EMs.

Main Methods:

  • Bioinformatic analysis of EMs- and m6A-related RNAs.
  • Establishment of mouse models for endometriosis (EMs) and mouse endometrial stromal cells (mESCs).
  • In vitro and in vivo experiments involving METTL3 and MIR17HG manipulation.

Main Results:

  • METTL3 and MIR17HG were found to be downregulated in an EMs mouse model.
  • Overexpression of METTL3 inhibited mESC proliferation, migration, and invasion.
  • METTL3 enhanced MIR17HG expression via m6A modification and suppressed E2 levels in EMs mice.

Conclusions:

  • METTL3 plays a protective role in endometriosis.
  • METTL3 prevents EMs progression by upregulating MIR17HG expression.
  • METTL3 influences key molecular pathways and hormone levels relevant to EMs.

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