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Related Concept Videos

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miR-520a-5p regulates Frizzled 9 expression and mediates effects of cigarette smoke and iloprost chemoprevention.

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Related Experiment Video

Updated: Mar 19, 2026

Isolation of Mouse Respiratory Epithelial Cells and Exposure to Experimental Cigarette Smoke at Air Liquid Interface
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Prostacyclin reverses the cigarette smoke-induced decrease in pulmonary Frizzled 9 expression through miR-31.

M A Tennis1, M L New1, D G McArthur2

  • 1University of Colorado Denver, Aurora, Colorado, USA.

Scientific Reports
|June 25, 2016
PubMed
Summary
This summary is machine-generated.

Former smokers with lung cancer can benefit from iloprost chemoprevention. This treatment requires Frizzled 9 (Fzd9) expression, which is reduced by smoking via miR-31, but restored by prostacyclin.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Pulmonology

Background:

  • Lung cancer is frequently diagnosed in former smokers, posing a significant clinical challenge.
  • Endobronchial dysplasia, a precancerous lung lesion, is prevalent in this population.
  • Prostacyclin analogue iloprost shows promise for chemoprevention in former smokers.

Purpose of the Study:

  • To investigate the interplay between cigarette smoke, Fzd9 expression, and iloprost efficacy.
  • To elucidate the molecular mechanisms underlying iloprost's chemopreventive action.
  • To identify potential biomarkers for iloprost therapy in former smokers.

Main Methods:

  • Analysis of human lung tumor and dysplasia samples.
  • In vivo studies using mouse models exposed to tobacco smoke.
  • In vitro experiments assessing gene expression and cellular responses.
  • Investigated the role of microRNA-31 (miR-31) in regulating Fzd9.

Main Results:

  • Fzd9 expression was found to be low in human lung tumors and progressive dysplasias.
  • Tobacco smoke carcinogens decreased Fzd9 expression in mouse models and in vitro.
  • Prostacyclin treatment maintained or increased Fzd9 expression.
  • miR-31 was identified as a repressor of Fzd9, an effect reversed by prostacyclin.
  • A model is proposed where smoking increases miR-31, reducing Fzd9 and iloprost response.

Conclusions:

  • Cigarette smoke downregulates Fzd9 via miR-31, hindering iloprost efficacy.
  • Cessation of smoking and prostacyclin treatment can restore Fzd9 expression.
  • Fzd9 and miR-31 are potential biomarkers for guiding iloprost chemoprevention.
  • Understanding these mechanisms can accelerate clinical trials and implementation of iloprost therapy.