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Proteasomes and RARS modulate AIMP1/EMAP II secretion in human cancer cell lines

Arianna Bottoni1, Cristina Vignali, Daniela Piccin

  • 1Section of Endocrinology, Department of Biomedical Sciences and Advanced Therapies, University of Ferrara, Ferrara, Italy.

Journal of Cellular Physiology
|April 20, 2007
PubMed

Insights

High RARS expression reduces AIMP1 secretion and EMAP II generation. Proteasome inhibition also impairs EMAP II production, revealing key regulatory roles in cytokine processing.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Aminoacyl t-RNA synthetase interacting multifunctional protein (AIMP1) is a precursor to the inflammatory cytokine endothelial monocyte-activating polypeptide II (EMAP II).
  • Previous studies suggested RARS (Ars) expression negatively correlates with AIMP1 secretion in pituitary adenomas.

Purpose of the Study:

  • To investigate the role of RARS in modulating AIMP1 secretion in HeLa and MCF7 cell lines.
  • To explore the involvement of the multicatalytic protease in cleaving AIMP1 to generate EMAP II.

Main Methods:

  • Over-expression of RARS in HeLa and MCF7 cells.
  • Proteasome inhibition experiments.
  • Analysis of AIMP1 secretion and EMAP II generation.

Main Results:

  • RARS over-expression significantly impaired AIMP1 secretion in both cell lines.
  • Proteasome inhibition hindered the cleavage of AIMP1 into EMAP II.
  • These findings link RARS levels to reduced AIMP1 secretion and protease activity to EMAP II formation.

Conclusions:

  • RARS over-expression is associated with decreased AIMP1 secretion.
  • The multicatalytic protease plays a crucial role in the generation of the mature cytokine EMAP II.

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