Proteasomes and RARS modulate AIMP1/EMAP II secretion in human cancer cell lines
Autor: | Daniela Piccin, Ettore C. degli Uberti, Arianna Bottoni, Andrea Luchin, Maria Chiara Zatelli, Cristina Vignali, Federico Tagliati |
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Rok vydání: | 2007 |
Předmět: |
Proteasome Endopeptidase Complex
Physiology medicine.medical_treatment Clinical Biochemistry Cell Uterine Cervical Neoplasms Breast Neoplasms Cysteine Proteinase Inhibitors Transfection Cleavage (embryo) Gene Expression Regulation Enzymologic HeLa medicine Humans Secretion Protease biology RNA-Binding Proteins Cell Biology Arginine-tRNA Ligase biology.organism_classification Molecular biology Acetylcysteine Neoplasm Proteins Gene Expression Regulation Neoplastic medicine.anatomical_structure Cytokine Proteasome Cell culture Cytokines Female Proteasome Inhibitors Protein Processing Post-Translational HeLa Cells |
Zdroj: | Journal of Cellular Physiology. 212:293-297 |
ISSN: | 0021-9541 |
DOI: | 10.1002/jcp.21083 |
Popis: | The aminoacyl t-RNA synthetase interacting multifunctional protein (AIMP1) is the precursor of the multifunctional inflammatory cytokine endothelial monocyte-activating polypeptide II (EMAP II). We previously demonstrated that AIMP1 secretion by pituitary adenomas is inversely correlated with tumor diameter and with RARS expression, suggesting that a high amount of RARS associated with AIMP1 might prevent the secretion of the latter cytokine. In this study, we investigated the role of RARS in modulating the secretion of AIMP1 in HeLa and MCF7 cell lines and investigated the possible role of the multicatalytic protease in the cleavage of AIMP1 to generate EMAP II. Our data show that RARS over-expression impairs AIMP1 secretion by both HeLa and MCF7 cells. Moreover, proteasome inhibition impairs AIMP1 cleavage to produce EMAP II. These data indicate that RARS over-expression associates with a reduced AIMP1 secretion and that the multicatalytic protease is involved in the generation of the mature cytokine, EMAP II. J. Cell. Physiol. 212: 293–297, 2007. © 2007 Wiley-Liss, Inc. |
Databáze: | OpenAIRE |
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