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MicroRNA circuits regulate the cancer-inflammation link

Dimitrios Iliopoulos1

  • 1Center for Systems Biomedicine, Division of Digestive Diseases, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA.

Science Signaling
|March 27, 2014
PubMed

Insights

A newly identified microRNA circuit, miR-146b, acts as an anti-inflammatory agent in breast cancer. Epigenetic silencing of this circuit in receptor-negative breast cancers promotes inflammation and cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Genetic and epigenetic changes drive cancer development.
  • Chronic inflammation is linked to oncogenesis, but the underlying molecular mechanisms remain unclear.
  • Inflammatory signaling pathways are frequently activated in various cancers.

Purpose of the Study:

  • To identify molecular circuits that sustain inflammatory factor activation in cancer.
  • To investigate the role of microRNAs in inflammation-driven oncogenesis.
  • To explore the epigenetic regulation of inflammatory circuits in breast cancer.

Main Methods:

  • High-throughput screening to identify signal transducer and activator of transcription 3 (STAT3)-regulated microRNAs.
  • Analysis of DNA methylation in microRNA promoter regions.
  • Overexpression of microRNA miR-146b in breast cancer cells.

Main Results:

  • MicroRNA miR-146b was identified as a direct STAT3 target in mammary epithelial cells.
  • DNA methylation suppressed miR-146b expression in cancer cells, indicating epigenetic repression.
  • Overexpression of miR-146b inhibited nuclear factor κB (NF-κB)-dependent IL6 expression, reduced STAT3 activation, and decreased cancer cell invasiveness and mesenchymal phenotype.

Conclusions:

  • A microRNA-mediated anti-inflammatory circuit involving miR-146b is epigenetically repressed in receptor-negative breast cancers.
  • This epigenetic silencing contributes to sustained inflammation and oncogenic transformation.
  • Targeting this circuit may offer therapeutic potential for estrogen receptor-negative breast cancers.

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