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Expression of Ras-related C3 botulinum toxin substrate 1 (RAC1) in human cholesteatoma

  • Otology
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European Archives of Oto-Rhino-Laryngology Aims and scope Submit manuscript

Abstract

Ras-related C3 botulinum toxin substrate 1 (RAC1) is a 21-kDa signaling G protein that functions as a pleiotropic regulator of many cellular processes including epithelial differentiation. RAC1 activates the nicotinamide adenine dinucleotide phosphate oxidase complex which promotes formation of reactive oxygen species and degradation enzymes. RAC1 has been associated with rapid epithelial differentiation and invasive properties in human cholesteatoma. This study aimed to identify the presence of RAC1 in human cholesteatoma and analyze its functional role as a regulator of proteolysis and overgrowth. Tissue samples from human cholesteatoma and normal postaural skin were obtained from patients during otologic surgery for cholesteatoma. The expression of RAC1 mRNA was quantified by real-time RT-PCR, and localization of RAC1 expression was confirmed using immunohistochemical staining. Expression of RAC1 mRNA in the epithelium of cholesteatoma was significantly elevated 2.94 fold on average, compared with normal control skin. RAC1 expression in the suprabasal and basal layer of cholesteatoma epithelium was stronger than normal control skin. Our results suggest that RAC1 can be associated with rapid epithelial differentiation and invasive properties of human cholesteatoma.

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Acknowledgments

This work was supported by the National Research Foundation of Korea Grant funded by the Korean Government MEST, Basic Research Promotion Fund (NRF-2010-013-E00015). This study was supported by the Brain Korea Project 21, and the Institutes of Communication Disorder at Korea University.

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The authors declare that they have no conflict of interest.

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Correspondence to Gi Jung Im.

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Lee, N.H., Chang, JW., Choi, J. et al. Expression of Ras-related C3 botulinum toxin substrate 1 (RAC1) in human cholesteatoma. Eur Arch Otorhinolaryngol 270, 455–459 (2013). https://doi.org/10.1007/s00405-012-1966-y

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  • DOI: https://doi.org/10.1007/s00405-012-1966-y

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