Expression patterns of p27(Kip1) and Ki-67 in cholesteatoma epithelium

Sungwon Chae, Jae-Jun Song, Han Kyu Suh, Hak Hyun Jung, Hyun Ho Lim, Soon Jae Hwang

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Objectives: The cell cycle must be involved in cell proliferation of the epithelium of middle ear cholesteatoma. Cyclins and cyclin-dependent kinase (CDK) complexes have important regulatory roles during cell cycle progression. Cyclin-CDK complexes are in turn regulated by the cyclin-dependent kinase inhibitors (CDKIs), which generally inhibit cell cycle progression. One of the important CDKI members is p27(Kip1). The goal of this study is to evaluate the expression of p27(Kip1) and Ki-67, a proliferation marker, in cholesteatoma and in the skin of the external ear canal. Methods: The expressions of p27(Kip1) and Ki-67 in cholesteatoma epithelium (n = 20) and ear canal epithelium (n = 7) were investigated by an immunohistochemical technique. Results: In cholesteatoma epithelium specimens, the expression of p27(Kip1) was observed from the parabasal layer to the granular layer, but not in the basal layer. Ki-67 was expressed dominantly in the basal and parabasal cell layers. Their expressions tend to be increased compared with their expressions in the normal ear canal skin. The expression pattern of the proliferation marker Ki-67 in the epithelial layers of two groups was inversely related to the expression of p27(Kip1) Conclusions: In cholesteatoma, the expressions of CDKI and Ki-67 were both increased in this study. The ability to inhibit proliferative activity was also increased in the cholesteatoma epithelium. The expression pattern of the proliferation marker Ki-67 in the epithelial layers was inversely related to the expression of p27(Kip1). Not only is the proliferation activity increased, but also the ability to inhibit hyperproliferation is increased in the cholesteatoma epidermis. Despite increased proliferative activity in the cholesteatoma epidermis, epithelial cells still retain the capability to prevent cell cycle arrest by means of p27(Kip1).

Original languageEnglish
Pages (from-to)1898-1901
Number of pages4
JournalLaryngoscope
Volume110
Issue number11
Publication statusPublished - 2000 Nov 23

Fingerprint

Cholesteatoma
Cyclin-Dependent Kinases
Epithelium
Ear Canal
Cell Cycle
Cyclins
Epidermis
Middle Ear Cholesteatoma
Skin
Cell Cycle Checkpoints
Epithelial Cells
Cell Proliferation

Keywords

  • Cholesteatoma
  • Cyclin-dependent kinase inhibitor
  • Ki-67
  • P27(Kip1)

ASJC Scopus subject areas

  • Otorhinolaryngology

Cite this

Expression patterns of p27(Kip1) and Ki-67 in cholesteatoma epithelium. / Chae, Sungwon; Song, Jae-Jun; Suh, Han Kyu; Jung, Hak Hyun; Lim, Hyun Ho; Hwang, Soon Jae.

In: Laryngoscope, Vol. 110, No. 11, 23.11.2000, p. 1898-1901.

Research output: Contribution to journalArticle

Chae, S, Song, J-J, Suh, HK, Jung, HH, Lim, HH & Hwang, SJ 2000, 'Expression patterns of p27(Kip1) and Ki-67 in cholesteatoma epithelium', Laryngoscope, vol. 110, no. 11, pp. 1898-1901.
Chae, Sungwon ; Song, Jae-Jun ; Suh, Han Kyu ; Jung, Hak Hyun ; Lim, Hyun Ho ; Hwang, Soon Jae. / Expression patterns of p27(Kip1) and Ki-67 in cholesteatoma epithelium. In: Laryngoscope. 2000 ; Vol. 110, No. 11. pp. 1898-1901.
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AU - Chae, Sungwon

AU - Song, Jae-Jun

AU - Suh, Han Kyu

AU - Jung, Hak Hyun

AU - Lim, Hyun Ho

AU - Hwang, Soon Jae

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AB - Objectives: The cell cycle must be involved in cell proliferation of the epithelium of middle ear cholesteatoma. Cyclins and cyclin-dependent kinase (CDK) complexes have important regulatory roles during cell cycle progression. Cyclin-CDK complexes are in turn regulated by the cyclin-dependent kinase inhibitors (CDKIs), which generally inhibit cell cycle progression. One of the important CDKI members is p27(Kip1). The goal of this study is to evaluate the expression of p27(Kip1) and Ki-67, a proliferation marker, in cholesteatoma and in the skin of the external ear canal. Methods: The expressions of p27(Kip1) and Ki-67 in cholesteatoma epithelium (n = 20) and ear canal epithelium (n = 7) were investigated by an immunohistochemical technique. Results: In cholesteatoma epithelium specimens, the expression of p27(Kip1) was observed from the parabasal layer to the granular layer, but not in the basal layer. Ki-67 was expressed dominantly in the basal and parabasal cell layers. Their expressions tend to be increased compared with their expressions in the normal ear canal skin. The expression pattern of the proliferation marker Ki-67 in the epithelial layers of two groups was inversely related to the expression of p27(Kip1) Conclusions: In cholesteatoma, the expressions of CDKI and Ki-67 were both increased in this study. The ability to inhibit proliferative activity was also increased in the cholesteatoma epithelium. The expression pattern of the proliferation marker Ki-67 in the epithelial layers was inversely related to the expression of p27(Kip1). Not only is the proliferation activity increased, but also the ability to inhibit hyperproliferation is increased in the cholesteatoma epidermis. Despite increased proliferative activity in the cholesteatoma epidermis, epithelial cells still retain the capability to prevent cell cycle arrest by means of p27(Kip1).

KW - Cholesteatoma

KW - Cyclin-dependent kinase inhibitor

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KW - P27(Kip1)

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