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The IKKα-regulated microRNA miR-9-5p mediates lung cancer growth and invasiveness via CDH1/Wnt/β-catenin signalling

Simoni Besta1,2, Eugenia Roupakia1,2, Zoi Kanaki3

  • 1Laboratory of Biology, School of Medicine, Faculty of Health Sciences, and Institute of Biosciences, Centre for Research and Innovation, University of Ioannina, University Campus, Ioannina, Greece.

Cell Death Discovery
|June 16, 2026
PubMed

Insights

Loss of IKKα in non-small cell lung cancer (NSCLC) upregulates oncogenic miR-9-5p. This microRNA promotes tumour growth and invasion by activating the Akt1/β-catenin pathway and driving epithelial-to-mesenchymal transition (EMT).

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signalling

Background:

  • IKKα acts as a tumour suppressor in non-small cell lung cancer (NSCLC) via NF-κB-independent pathways.
  • Downstream signalling of IKKα in NSCLC remains largely uncharacterized.

Purpose of the Study:

  • To investigate the downstream signalling pathways regulated by IKKα in NSCLC.
  • To identify microRNAs (miRNAs) affected by IKKα depletion in NSCLC cells.

Main Methods:

  • Silencing of IKKα in NSCLC cells.
  • Nanostring miRNome analysis to profile miRNA expression.
  • In vitro assays for cell migration, invasion, and epithelial-to-mesenchymal transition (EMT).
  • In vivo tumour xenograft models in mice.

Main Results:

  • IKKα depletion led to significant upregulation of the oncomiR miR-9-5p.
  • Overexpression of miR-9-5p enhanced NSCLC cell migration, invasion, and induced EMT.
  • miR-9-5p activated the Akt1/β-catenin pathway and promoted tumour growth in vivo.
  • Transcriptomic analysis revealed altered gene expression related to EMT, apoptosis, and NF-κB signalling.

Conclusions:

  • miR-9-5p functions as an oncogenic effector following IKKα loss in NSCLC.
  • miR-9-5p promotes tumour progression, invasiveness, and growth through EMT and Akt-1/GSK-3β/β-catenin pathway activation.

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