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Epigenetic regulation of microRNA expression in renal cell carcinoma

Miriam Schiffgen1, Doris H Schmidt, Alexander von Rücker

  • 1Klinik und Poliklinik für Urologie und Kinderurologie, Universitätsklinikum Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. miriam.schiffgen@gmx.de

Biochemical and Biophysical Research Communications
|May 28, 2013
PubMed

Insights

Epigenetic drugs re-expressed silenced microRNAs in renal cell carcinoma. This suggests a therapeutic strategy targeting microRNA restoration for cancer treatment.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • MicroRNA deregulation is a hallmark of cancer, contributing to carcinogenesis.
  • Epigenetic modifications, including DNA methylation and histone acetylation, are key mechanisms underlying microRNA dysregulation.

Purpose of the Study:

  • To investigate the role of epigenetic modifications in microRNA deregulation in renal cell carcinoma (RCC).
  • To determine if epigenetic drugs can restore the expression of silenced tumor-suppressive microRNAs in ccRCC cell lines.

Main Methods:

  • Treatment of ccRCC cell lines with DNA-methyltransferase inhibitor (5-aza-2'-deoxycytidine) and histone-deacetylase inhibitor (suberoylanilide hydroxamic acid).
  • Analysis of microRNA expression levels and epigenetic modifications at microRNA promoters (e.g., H3 and H3K18 acetylation, DNA methylation).

Main Results:

  • Treatment with epigenetic drugs induced the expression of numerous microRNAs in ccRCC cell lines.
  • Re-expression of miR-9 was associated with enrichment of H3 and H3K18 acetylation at its promoter, while DNA hypermethylation remained unchanged.
  • Silenced microRNAs with potential tumor-suppressive functions were re-expressed following epigenetic drug treatment.

Conclusions:

  • Epigenetic modifications, particularly histone acetylation, are crucial for the re-expression of silenced microRNAs in ccRCC.
  • Epigenetic drug treatment can restore tumor-suppressive microRNA expression, offering a potential therapeutic avenue for ccRCC.

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