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MiR-126-3p suppresses the growth, migration and invasion of NSCLC via targeting CCR1

R Liu1, Y-S Zhang, S Zhang

  • 1Medical Image Institute, Guizhou Medical University, Guiyang, Guizhou, China. 1483982032@qq.com.

European Review for Medical and Pharmacological Sciences
|February 6, 2019
PubMed
Abstract

Insights

MicroRNA 126-3p (miR-126-3p) is down-regulated in non-small-cell lung cancer (NSCLC). Restoring miR-126-3p inhibits NSCLC growth and metastasis by targeting chemokine receptor 1 (CCR1).

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are crucial regulators in cancer development.
  • Non-small-cell lung cancer (NSCLC) progression involves complex molecular mechanisms.
  • Understanding specific miRNA roles, like miR-126-3p, is vital for NSCLC research.

Purpose of the Study:

  • To investigate the functional role of miR-126-3p in non-small-cell lung cancer (NSCLC) cell growth and metastasis.
  • To identify the molecular targets and pathways regulated by miR-126-3p in NSCLC.

Main Methods:

  • Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) for miRNA expression analysis.
  • In vitro assays (MTT, colony formation, wound healing, transwell invasion) to assess cell behavior.
  • Immunofluorescence staining for epithelial-mesenchymal transition (EMT) markers.
  • In vivo studies using xenograft and lung metastasis models in mice.

Main Results:

  • miR-126-3p expression was significantly reduced in NSCLC cell lines and tissues.
  • Upregulation of miR-126-3p suppressed NSCLC cell proliferation, migration, and invasion.
  • miR-126-3p inhibited NSCLC growth and metastasis in vivo by targeting chemokine (C-C motif) receptor 1 (CCR1).
  • CCR1 overexpression reversed the inhibitory effects of miR-126-3p, while CCR1 knockdown mimicked these effects.

Conclusions:

  • miR-126-3p acts as a tumor suppressor in non-small-cell lung cancer.
  • The miR-126-3p/CCR1 axis is a key regulator of NSCLC progression, including growth, migration, and invasion.
  • Targeting the miR-126-3p pathway may offer therapeutic strategies for NSCLC.

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