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Circular RNA circCRIM1 suppresses lung adenocarcinoma cell migration, invasion, EMT, and glycolysis through

S-J Zhang1, J Ma, J-C Wu

  • 1Department of Respiratory, Huaihe Hospital of Henan University, Kaifeng, China. zsj9224@163.com.

European Review for Medical and Pharmacological Sciences
|April 25, 2020
PubMed
Abstract

Insights

Circular RNA circCRIM1 is downregulated in lung adenocarcinoma (LUAC). Upregulating circCRIM1 suppresses LUAC progression by targeting miR-125b-5p and enhancing BTG2 expression, offering a potential diagnostic and therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Circular RNAs (circRNAs) are implicated in human cancers.
  • Lung adenocarcinoma (LUAC) is characterized by a high rate of metastasis.
  • Understanding the role of specific circRNAs in LUAC is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the function and mechanism of circular RNA circCRIM1 in the development of LUAC.
  • To explore the regulatory network involving circCRIM1, miR-125b-5p, and BTG2 in LUAC.

Main Methods:

  • Quantitative Real-time polymerase chain reaction (qRT-PCR) and Western blot were used to assess molecular levels.
  • Transwell assays evaluated cell migration and invasion.
  • In vivo studies utilized mouse xenograft models to assess tumor growth.
  • Dual-luciferase reporter assays confirmed target interactions.

Main Results:

  • CircCRIM1 and BTG2 were downregulated, while miR-125b-5p was upregulated in LUAC tissues and cells.
  • CircCRIM1 upregulation inhibited LUAC cell migration, invasion, epithelial-mesenchymal transition (EMT), glycolysis, and tumor growth.
  • CircCRIM1 acts as a sponge for miR-125b-5p, thereby increasing BTG2 expression and suppressing LUAC progression.

Conclusions:

  • CircCRIM1 is lowly expressed in LUAC and suppresses tumor development by sponging miR-125b-5p to enhance BTG2 expression.
  • CircCRIM1 holds potential as a biomarker and therapeutic target for LUAC patients.

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