Abstract
PurposeIn humans, activation-induced cytidine deaminase (AID) expression results due to inflammation and this deaminase activity is also involved in carcinogenesis. The aim of this study is to investigate the correlation between AID expression and the clinical classification of oral cancer tissues.Experimental DesignThe current study investigated the correlation between AID expression and the clinical classification of oral cancer tissues from 27 patients who underwent surgical resection using immunohistochemistry. Specific AID expression and its induction by cytokine stimulation were investigated in cultured HSC oral cancer cell lines by reverse transcriptase PCR.ResultsAID expression was detected in 10 of 27 specimens (37.0%). AID expression was more frequently detected in early-stage cancer, especially in early stage T, than in late-stage cancer (T1/T2 vs. T3/4; P = 0.0493, N0 vs. N1/2/3; P = 0.0793). HSC-2, a nonmetastatic oral cancer cell line, abundantly expressed endogenous AID, whereas no such expression was observed in HSC-3, a metastatic oral cancer cell line. Moreover, AID expression was substantially induced in HSC-2 cells by stimulation of an inflammation-related cytokine, TNF-α.ConclusionsAberrant AID expression in the oral epithelium would contribute to the initiation of oral squamous cell carcinoma. Avoiding persistent AID inducible condition such as frequent cleaning of oral cavity would play an important role for the prevention of developing oral cancer.
Highlights
Head and neck cancer is the sixth most common malignancy worldwide [1]
activation-induced cytidine deaminase (AID) expression was more frequently detected in earlystage cancer, especially in early stage T, than in late-stage cancer (T1/T2 vs. T3/4; P = 0.0493, N0 vs. N1/2/3; P = 0.0793)
HSC2, a nonmetastatic oral cancer cell line, abundantly expressed endogenous AID, whereas no such expression was observed in HSC-3, a metastatic oral cancer cell line
Summary
Head and neck cancer is the sixth most common malignancy worldwide [1]. 25% oral cancers are attributable to tobacco use (smoking and/or chewing), 7%–19% to alcohol consumption, 10%–15% to micronutrient deficiency, and more than 50% to betel quid chewing in areas of high chewing prevalence [4]. Correlations have been reported between metastatic tumor recurrence and expression of metastasispromoting factors such as matrix metalloproteinases (MMPs), tissue inhibitors of MMP-2 (TIMP-2), Ets-1, and autocrine motility factor in patients with tongue squamous cell carcinoma [5,6,7]. We have reported the correlation between TIMP-2 expression and MMP-2 expression and have predicted a poor prognosis in patients with squamous cell carcinoma of the tongue [7]. The mechanisms by which oral squamous cells undergo genetic changes, which subsequently lead to their malignant transformation remain unknown
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