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The Tumor Suppressive mir-148a Is Epigenetically Inactivated in Classical Hodgkin Lymphoma

Julia Paczkowska1, Joanna Janiszewska1, Julia Bein2

  • 1Institute of Human Genetics, Polish Academy of Sciences, 60-479 Poznan, Poland.

Cells
|October 17, 2020
PubMed

Insights

Epigenetic silencing of microRNAs (miRNAs) is common in classical Hodgkin lymphoma (cHL). We identified mir-148a as a novel tumor suppressor inactivated by DNA methylation in cHL, reducing cell proliferation.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Oncology

Background:

  • DNA methylation is critical for transcriptional deregulation in classical Hodgkin lymphoma (cHL) pathogenesis.
  • MicroRNAs (miRNAs) play a role in gene regulation and cancer development.
  • Identifying epigenetically silenced miRNAs in cHL is crucial for understanding disease mechanisms.

Purpose of the Study:

  • To identify epigenetically inactivated miRNAs in cHL.
  • To investigate the functional role of identified miRNAs in cHL.
  • To explore the therapeutic potential of miRNA restoration in cHL.

Main Methods:

  • Analysis of downregulated miRNAs in cHL cell lines using bisulfite pyrosequencing.
  • Focus on miRNAs with promoter regions near CpG islands.
  • Validation in primary Hodgkin and Reed-Sternberg (HRS) cells via laser capture microdissection.
  • Luciferase reporter assays to confirm miRNA:mRNA interactions.
  • Establishment of cHL cell lines with stable miRNA overexpression for proliferation tests.

Main Results:

  • Significant inverse correlation between DNA methylation and expression of mir-339-3p, mir-148a-3p, mir-148a-5p, and mir-193a-5p.
  • Demonstrated direct interaction of miR-148a-3p with IL15 and HOMER1 transcripts.
  • Demonstrated direct interaction of miR-148a-5p with SUB1 and SERPINH1 transcripts.
  • Overexpression of mir-148a led to reduced proliferation in KM-H2 cHL cell line.

Conclusions:

  • Epigenetic silencing of miRNAs is a common phenomenon in cHL.
  • mir-148a is a novel tumor suppressor inactivated in cHL.
  • Restoration of mir-148a function may represent a potential therapeutic strategy for cHL.
Keywords:
DNA methylationcHLepigeneticmicroRNAmir-148a

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