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c-Fos-dependent miR-22 targets MDC1 and regulates DNA repair in terminally differentiated cells

Jung-Hee Lee1,2, Seon-Joo Park1,3, Seok Won Kim4

  • 1Laboratory of Genomic Instability and Cancer Therapeutics, Cancer Mutation Research Center, Chosun University School of Medicine, Seosuk-dong, Gwangju, Republic of Korea.

Oncotarget
|June 22, 2017
PubMed

Insights

Terminally differentiated cells show impaired DNA repair due to increased miR-22, which downregulates MDC1. Restoring MDC1 levels rescues double-stranded break (DSB) repair capacity in these cells.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Terminally differentiated cells exhibit diminished DNA double-stranded break (DSB) repair capacity.
  • The molecular mechanisms underlying this reduced repair efficiency are not fully understood.

Purpose of the Study:

  • To investigate the role of miR-22 in regulating DNA repair in terminally differentiated cells.
  • To elucidate the molecular pathway involving miR-22, MDC1, and c-Fos in DNA damage response.

Main Methods:

  • Analysis of miR-22 and MDC1 expression during differentiation of human breast (MCF-7) and hematopoietic (HL60, K562) cells.
  • Investigating the effect of miR-22 inhibition and c-Fos knockdown on DSB repair and MDC1 recruitment after ionizing radiation (IR).

Main Results:

  • miR-22 is upregulated in differentiated cells, correlating with decreased MDC1 expression and impaired DSB repair.
  • Inhibition of miR-22 restored MDC1 levels and fully rescued DSB repair.
  • Knockdown of c-Fos also rescued MDC1 levels, foci formation, and DSB repair efficiency.

Conclusions:

  • The c-Fos/miR-22/MDC1 axis is crucial for DNA repair in terminally differentiated cells.
  • Understanding this pathway offers insights into the reduced DNA repair capacity observed in differentiated cells.
Keywords:
DNA repairMDC1c-FosdifferentiationmiR-22

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