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Updated: Nov 14, 2025

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
08:56

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues

Published on: December 5, 2016

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N-methyladenosine reader YTHDF2-mediated long noncoding RNA FENDRR degradation promotes cell proliferation in

Jie Shen1, Xiao-Ping Feng1,2, Ru-Bing Hu2

  • 1Department of Gynecology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.

Laboratory Investigation; a Journal of Technical Methods and Pathology
|March 11, 2021
PubMed

Insights

Dysregulation of long noncoding RNA (LncRNA) FENDRR is linked to cancer. In endometrioid endometrial carcinoma (EEC), YTHDF2 degrades FENDRR, promoting cancer growth by increasing SOX4. Restoring FENDRR inhibits EEC progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Long noncoding RNA (LncRNA) FENDRR dysregulation is implicated in various cancers.
  • The specific role and regulatory mechanisms of FENDRR in endometrioid endometrial carcinoma (EEC) are not well understood.

Purpose of the Study:

  • To investigate the role of LncRNA FENDRR in EEC progression.
  • To elucidate the upstream regulatory mechanism involving N-methyladenosine (m6A) modification and its associated proteins.

Main Methods:

  • Analysis of LncRNA FENDRR expression and m6A methylation in EEC patient tissues and cell lines.
  • In vitro studies using EEC cell lines (HEC-1B) to assess the effects of FENDRR and YTHDF2 manipulation on cell proliferation and apoptosis.
  • In vivo xenograft mouse models to evaluate the impact of FENDRR overexpression on tumor growth.

Main Results:

  • LncRNA FENDRR expression was decreased, while its m6A methylation was elevated in EEC tissues.
  • YTH domain-containing 2 (YTHDF2) recognized and promoted the degradation of m6A-modified FENDRR in EEC cells.
  • FENDRR overexpression suppressed proliferation and induced apoptosis by reducing SOX4 protein levels.
  • In vivo studies confirmed that FENDRR overexpression inhibited EEC cell growth.

Conclusions:

  • YTHDF2-mediated degradation of LncRNA FENDRR promotes EEC cell proliferation by upregulating SOX4 expression.
  • FENDRR acts as a tumor suppressor in EEC, and its degradation by YTHDF2 is a key mechanism in EEC progression.

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