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Polymorphic mature microRNAs from passenger strand of pre-miR-146a contribute to thyroid cancer

Krystian Jazdzewski1, Sandya Liyanarachchi, Michal Swierniak

  • 1Human Cancer Genetics Program, Comprehensive Cancer Center and Division of Endocrinology, Ohio State University, Columbus, OH 43210, USA.

Proceedings of the National Academy of Sciences of the United States of America
|January 24, 2009
PubMed

Insights

Genetic variations in microRNA-146a precursor (SNP rs2910164) increase thyroid cancer risk by producing extra microRNAs from the passenger strand, impacting apoptosis and DNA damage response.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Single nucleotide polymorphism (SNP rs2910164) in microRNA-146a precursor is linked to papillary thyroid carcinoma (PTC) risk.
  • The underlying mechanism for this predisposition remained unclear.

Purpose of the Study:

  • To elucidate the mechanism by which microRNA-146a precursor heterozygosity (G/C) predisposes to PTC.
  • To investigate the role of passenger strand microRNAs in cancer development.

Main Methods:

  • TaqMan analysis of paired tumor/normal thyroid samples.
  • Microarray analysis of gene expression in tumor and normal thyroid tissues.
  • Analysis of microRNA production from different genotypes (GG, GC, CC).

Main Results:

  • GC heterozygotes produce three mature microRNAs, including two from the passenger strand (miR-146a*G and miR-146a*C).
  • Polymorphic miR-146a* showed 1.5- to 2.6-fold overexpression in 7 of 8 PTC tumors.
  • Microarray data revealed distinct transcriptomes in tumors and normal tissues based on genotype, with modulated genes involved in apoptosis and DNA damage response.

Conclusions:

  • Passenger strand microRNA transcripts can significantly influence downstream gene effects.
  • Heterozygosity in premiR sequences can lead to epistasis via additional mature microRNA production.
  • Mature microRNAs from the passenger strand may play a crucial role in regulating genetic processes and cancer predisposition.

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