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QKI, a miR-200 target gene, suppresses epithelial-to-mesenchymal transition and tumor growth

Eun Ju Kim1, Jeong Seon Kim1, Sieun Lee1

  • 1Department of Molecular Medicine and Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, South Korea.

International Journal of Cancer
|April 27, 2019
PubMed

Insights

The microRNA-200 (miR-200) family targets the quaking (QKI) protein, a tumor suppressor. QKI suppresses epithelial-to-mesenchymal transition (EMT) and tumorigenesis, forming a feedback loop with miR-200 in oral squamous cell carcinoma.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • The microRNA-200 (miR-200) family inhibits epithelial-to-mesenchymal transition (EMT) by targeting ZEB1/ZEB2 transcription factors.
  • EMT is crucial in tumor progression, particularly in oral squamous cell carcinoma (OSCC).
  • Quaking (QKI) is a newly identified RNA-binding protein and potential tumor suppressor regulated during EMT.

Purpose of the Study:

  • To investigate the regulatory relationship between the miR-200 family and QKI in OSCC.
  • To determine if QKI acts as a tumor suppressor by modulating EMT.

Main Methods:

  • Bioinformatic analysis (TargetScan, TCGA) to predict miR-200 binding sites on QKI 3'-UTR.
  • In vitro experiments: forced miR-200 expression in OSCC cell lines (CAL27, HSC3) to assess effects on ZEB1/2, cell migration, and QKI levels.
  • Luciferase reporter assays to confirm direct targeting of QKI 3'-UTR by miR-200.
  • In vitro and in vivo studies using shRNA-mediated QKI knockdown to evaluate its role in EMT and tumorigenesis.
  • Analysis of QKI protein expression in patient cohorts (HNSCC, lung adenocarcinoma) and correlation with prognosis.

Main Results:

  • miR-200 family members (miR-200b/a/429) inhibited ZEB1/2 expression and reduced cell migration in OSCC cells.
  • miR-200 overexpression suppressed QKI expression, and direct targeting of QKI 3'-UTR by miR-200 was confirmed.
  • QKI knockdown promoted EMT and protumor effects in vitro and in vivo.
  • High QKI protein expression correlated with better prognosis in HNSCC and lung adenocarcinoma patients.

Conclusions:

  • QKI is upregulated during EMT and is a direct target of the miR-200 family.
  • QKI functions as a tumor suppressor by inhibiting EMT and tumorigenesis.
  • A negative feedback loop exists between QKI and miR-200, crucial for maintaining cellular homeostasis against EMT-inducing signals.
Keywords:
QKIepithelial-to-mesenchymal transitionlung cancermiRNA-200oral cancer

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