Circ-IGF1R inhibits cell invasion and migration in non-small cell lung cancer

Zhanyu Xu1, Weiwei Xiang1, Wenjie Chen1

  • 1Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.

Thoracic Cancer
|February 29, 2020
PubMed
Abstract

Insights

Circular RNA (circ-IGF1R) is downregulated in lung cancer, inhibiting tumor invasion and migration. This study elucidates its mechanism via the circ-IGF1R-miR-1270-VANGL2 network, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Circular RNAs (circRNAs) are emerging biomarkers for tumor invasion and migration.
  • The specific role of hsa_circ_0005035 (circ-IGF1R) in non-small cell lung cancer (NSCLC) requires elucidation.

Purpose of the Study:

  • To investigate the mechanism of action of circ-IGF1R in lung cancer.
  • To determine the association between circ-IGF1R expression and NSCLC progression.

Main Methods:

  • Screening of circ-IGF1R from the Gene Expression Omnibus database (GSE104854).
  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) to assess circ-IGF1R expression in NSCLC cell lines and tissues.
  • Wound-healing and Transwell assays to evaluate the functional role of circ-IGF1R.
  • RNA-sequencing (RNA-seq) to explore the circ-IGF1R-mediated transcriptome changes.

Main Results:

  • circ-IGF1R expression was significantly lower in lung cancer tissues and cell lines compared to normal controls (P < 0.0001).
  • Reduced circ-IGF1R levels correlated with advanced tumor stage (T2/T3/T4) and lymph node metastasis (N1/N2/N3) (P < 0.05).
  • Overexpression of circ-IGF1R suppressed lung cancer cell invasion and migration.

Conclusions:

  • circ-IGF1R acts as a tumor suppressor in lung cancer.
  • The inhibitory effect on invasion and migration is potentially mediated by the circ-IGF1R-miR-1270-VANGL2 axis.
  • circ-IGF1R represents a promising molecular marker and therapeutic target for NSCLC.

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