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Mex-3B induces apoptosis by inhibiting miR-92a access to the Bim-3'UTR

Takeaki Oda1, Yusuke Yamazumi1, Takatoshi Hiroko1

  • 1Laboratory of Molecular and Genetic Information, Institute for Molecular and Cellular Biosciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-0032, Japan.

Oncogene
|June 1, 2018
PubMed

Insights

Mex-3B protein regulates DNA damage response by upregulating the pro-apoptotic Bim protein. This RNA-binding protein prevents miR-92a from binding to Bim, promoting apoptosis during cellular stress.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Cells activate stress responses, including apoptosis, upon DNA damage.
  • MicroRNAs (miRNAs) regulate gene expression post-transcriptionally, impacting cellular processes.
  • RNA-binding proteins control miRNA activity and biogenesis.

Purpose of the Study:

  • To investigate the role of Mex-3B in DNA stress-induced apoptosis.
  • To elucidate the posttranscriptional mechanisms involving Mex-3B, Bim, and miRNAs.

Main Methods:

  • Investigated the function of Mex-3B in cellular stress responses.
  • Analyzed the interaction between Mex-3B, Bim mRNA, and miR-92a.
  • Utilized molecular biology techniques to study posttranscriptional gene regulation.

Main Results:

  • Mex-3B upregulates the pro-apoptotic Bim protein during DNA stress.
  • Mex-3B binds to the Bim 3'-untranslated region (3'UTR).
  • Mex-3B binding inhibits the interaction of Argonaute (Ago)-miR-92a with Bim RNA.

Conclusions:

  • Mex-3B plays a critical role in DNA stress-induced apoptosis.
  • Mex-3B modulates Bim expression by interfering with miRNA binding.
  • This study reveals novel posttranscriptional regulatory mechanisms in cellular stress responses.

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