LncRNA RUNX1-IT1 is Downregulated in Endometrial Cancer and Binds to miR-21 Precursor to Suppress Its Maturation

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Updated: Nov 22, 2025

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
08:40

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library

Published on: April 6, 2012

17.8K

Minglin Liang1, Hongbo Wang1, Cong Liu1

  • 1Department of Obstetrics and Gynecology, Union Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology, Wuhan City, Hubei Province 430022, People's Republic of China.

Cancer Management and Research
|January 7, 2021
PubMed
Abstract

Insights

RUNX1-IT1 is downregulated in endometrial cancer (EC) and suppresses tumor growth. It inhibits EC cell proliferation by reducing the maturation of miR-21, a key cancer-promoting microRNA.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • RUNX1-IT1 is known to suppress colorectal and liver cancers.
  • Its function in endometrial cancer (EC) remains largely unexplored.

Purpose of the Study:

  • To investigate the role and mechanism of RUNX1-IT1 in endometrial cancer.
  • To determine the relationship between RUNX1-IT1 and miR-21 in EC.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) to measure gene and microRNA expression in EC tissues and cells.
  • Dual-luciferase reporter assays and RNA pull-down assays to confirm molecular interactions.
  • Cell Counting Kit-8 (CCK-8) assay to assess cell proliferation.

Main Results:

  • RUNX1-IT1 expression is significantly downregulated in EC tissues compared to normal tissues.
  • RUNX1-IT1 inversely correlates with mature miR-21 levels in EC.
  • Overexpression of RUNX1-IT1 in EC cells suppresses cell proliferation by inhibiting miR-21 maturation.

Conclusions:

  • RUNX1-IT1 acts as a tumor suppressor in endometrial cancer.
  • RUNX1-IT1 inhibits EC cell proliferation through the suppression of miR-21 maturation.
Keywords:
RUNX1-IT1endometrial cancermiR-21precursorproliferation

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