BMC Oral Health (Jul 2019)
Overexpression of Epstein-Barr virus-encoded latent membrane protein-1 (LMP-1) in oral squamous cell carcinoma
Abstract
Abstract Background As oral cavity is the main location of Epstein-Barr virus (EBV) latency and shedding, and as EBV-encoded latent membrane protein-1 (LMP-1) has a crucial role in cell transformation, association between EBV infection, LMP-1 expression and oral malignancy is of interest. Although EBV DNA has been detected in oral squamous cell carcinoma (OSCC), studies on LMP-1 expression in OSCC and oral potentially malignant disorders are scarce and still controversial. This study aimed to evaluate the expression of LMP-1 in OSCC and oral leukoplakia (OL). Methods Biopsy specimens of 36 OSCC, 69 OL with and without dysplasia and 10 normal oral mucosa were assessed for the expression of LMP-1 using immunohistochemistry. In each case, at least 1000 cells were counted. Cells with staining were considered positive, classified by location as nuclear, cytoplasmic and nuclear plus cytoplasmic staining. Percentage of positive cells at different locations and of total positive cells were determined. For statistical analysis, SPSS version 21 was used. Statistical significance was considered at p < 0.05. Results LMP-1 was expressed in all studied specimens. In terms of percentage of total positive cells, LMP-1 expression was higher from normal mucosa (26.36%), OL without dysplasia (28.03%), OL with dysplasia (34.15%), to the significantly highest, (59.67%) in OSCC. In addition, cells with nuclear staining alone, cytoplasmic staining alone and cells with nuclear plus cytoplasmic staining were significantly higher in OSCC compared to those of normal mucosa, OL with and without dysplasia. Conclusions LMP-1 was overexpressed in OSCC. Our analysis on subcellular localization of LMP-1 in OSCC revealed prominent distinguished pattern, cytoplasmic distribution. Further studies in cell lines and animals are required to clarify the association between this EBV-encoded proteins and oral carcinogenesis.
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