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YTHDF2, a protein repressed by miR-145, regulates proliferation, apoptosis, and migration in ovarian cancer cells

Jie Li1, Lei Wu2, Meili Pei2

  • 1Department of Pathology, the First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, 710061, Shaanxi, China. lijiexj64@126.com.

Journal of Ovarian Research
|September 19, 2020
PubMed

Insights

YTHDF2 promotes epithelial ovarian cancer (EOC) by reducing m6A levels, while miR-145 counteracts this. This YTHDF2 and miR-145 feedback loop offers potential therapeutic targets for EOC.

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Oncology

Background:

  • RNA methylation, specifically N6-methyladenosine (m6A), is a critical epigenetic modification.
  • The role of YTHDF2, an m6A reader, in epithelial ovarian cancer (EOC) progression remains unclear.
  • Understanding m6A regulators is vital for EOC research.

Purpose of the Study:

  • To investigate the roles of YTHDF2 and miR-145 in EOC progression via m6A modification.
  • To elucidate the regulatory mechanism between YTHDF2 and miR-145 in EOC.
  • To identify potential therapeutic targets for EOC.

Main Methods:

  • Expression analysis of YTHDF2 and miR-145 in EOC tissues and cell lines.
  • Functional studies assessing the impact of YTHDF2 on EOC cell proliferation and migration.
  • Investigation of the regulatory relationship and feedback loop between YTHDF2 and miR-145.

Main Results:

  • YTHDF2 is upregulated in EOC and promotes tumor cell proliferation and migration.
  • YTHDF2 overexpression reduces global m6A mRNA levels in EOC cells.
  • A negative feedback loop exists between miR-145 and YTHDF2, with YTHDF2 being a direct target of miR-145.

Conclusions:

  • YTHDF2 and miR-145 act as key m6A regulators involved in EOC progression.
  • The interplay between YTHDF2 and miR-145 indirectly modulates m6A levels, influencing EOC development.
  • These findings highlight YTHDF2 and miR-145 as potential therapeutic targets for EOC.
Keywords:
Ovarian cancerYTHDF2m6AmiR-145

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