Expression of the human homolog of discs, large homolog 1 (Drosophila) in normal epithelium, nodule, papilloma and invasive squamous cell carcinoma of larynx

Sun-ju Byeon, Wook Youn Kim, Kyung Yeol Lee, Tae Sook Hwang, Young Ho Kim, Mee Soo Chang
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引用次数: 1

Abstract

Background and aim: The discs large 1 of Drosophila (DLG1) is a cell junction-localized protein that is required for the maintenance of cyto-architectural stability and alteration of DLG1 may be related to development of epithelial neoplasm. Methods: To determine DLG1 expression in human papillomavirus-related carcinogenesis, DLG1 expression in normal larynx (NL), laryngeal nodule (LN), laryngeal papilloma (LP), and invasive squamous cell carcinoma of larynx (SQCC) was investigated using immunohistochemistry. Results: In LN, the expression pattern of DLG1 was similar to NL showing cytoplasmic expression of basal and suprabasal cells except suprabasal membranous staining, which is observed in NL. In regard to basal cell expression, unlikely NL and LN, and the basal cells of most LPs did not express DLG1. In SQCC, the cancer cells of surface area showed strong cytoplasmic and membranous staining patterns of DLG1 in most SQCCs, whereas cells of deep invasive edge (IE) demonstrated weak cytoplasmic patterns without membranous staining. This expression pattern of DLG1 was similar to that of E-cadherin. Conclusions: Weak expression of DLG1 in IE of SQCC with a pattern similar to E-cadherin suggests that the perturbation of DLG1 as cell junction-localized cyto-architectural protein may be associated with progression of invasiveness.

人盘状同源物、大同源物1(果蝇)在喉部正常上皮、结节、乳头状瘤和浸润性鳞癌中的表达
背景与目的:果蝇的大圆盘1 (DLG1)是一种细胞连接定位蛋白,是维持细胞结构稳定性所必需的,DLG1的改变可能与上皮肿瘤的发生有关。方法:为检测DLG1在人乳头瘤病毒相关癌变中的表达,采用免疫组化方法检测DLG1在正常喉(NL)、喉结节(LN)、喉乳头状瘤(LP)和喉部浸润性鳞状细胞癌(SQCC)中的表达。结果:在LN中,DLG1的表达模式与NL相似,除基底上膜染色外,均为基底细胞和基底上细胞的细胞质表达。基底细胞表达方面,NL和LN不太可能,大部分LPs的基底细胞不表达DLG1。在SQCC中,大多数SQCC表面癌细胞表现出较强的DLG1细胞质和膜性染色模式,而深浸润边缘(IE)细胞表现出较弱的细胞质模式,无膜性染色。DLG1的表达模式与E-cadherin相似。结论:DLG1在SQCC IE中的弱表达模式与E-cadherin相似,提示DLG1作为细胞连接定位的细胞结构蛋白的紊乱可能与侵袭进展有关。
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