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Updated: Jun 13, 2026

Evaluation of Planar-Cell-Polarity Phenotypes in Ciliopathy Mouse Mutant Cochlea
Published on: February 21, 2016
Expression of CYLD and NF-kappaB in human cholesteatoma epithelium
Jae Yong Byun1, Tae Young Yune, Jee Youn Lee
1Department of Otolaryngology, School of Medicine, Kyung Hee University, Seoul, South Korea. otorhino512@naver.com
Abstract:
The tumor suppressor CYLD is a deubiquitinating enzyme that inhibits activation of the NF-kappaB, which has key roles in inflammation and apoptosis. We hypothesized that CYLD may regulate the NF-kappaB signaling pathway in cholesteatoma. We conducted immunohistochemistry to examine the expression of CYLD and NF-kappaB in 16 cases of cholesteatoma and paired cases of retroauricular (RA) skin. In cholesteatoma epithelium, activated NF-kappa B expression was significantly higher than in RA skin, whereas CYLD expression was significantly lower in cholesteatoma epithelium than in RA skin (P < .05). Furthermore, a significant inverse correlation was detected between CYLD and activated NF-kappaB expression in cholesteatoma epithelium (r = -0.630). We found that CYLD reduced and activated increased NF-kappaB in cholesteatoma epithelium in comparison to RA skin. The inverse correlation between CYLD and activated NF-kappaB in cholesteatoma may be involved in cholesteatoma epithelial hyperplasia.
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