Expression of histone deacetylase 2 (HDAC 2) in oral cancer patients
Date Issued
2009
Date
2009
Author(s)
Chang, Hao-Hueng
Abstract
Histone deacetylase 2 (HDAC2) has been implicated in the development and progression of several human tumors. We immunohistochemically examined the expression of HDAC2 protein in 20 cases of oral epithelial dysplasia (OED) and 93 cases of oral squamous cell carcinoma (OSCC). Positive HDAC2 nuclear staining was observed in 80 of the 93 (86%) cases of SCC and 11 of the 20 (55%) cases of ED. The labeling index (LI) for HDAC2 nuclear staining increased significantly from ED (25.8 ± 26.5%) to SCCs (59.8 ± 28.5%) (p < 0.001). No significant correlation was found between the HDAC2 expression level and patient''s age, sex, and oral habits in oral SCC patients. However, cancer with advanced stage, larger tumor size, or positive lymph node metastasis had higher level of HDAC2 protein expression. Kaplan-Meier curves showed oral SCC patients with high HDAC2 expression (LI >50 %), advanced stage, larger tumor size, or positive lymph node metastasis had significantly shorter overall survival (p=0.0158, 0.0267, 0.0029 and 0.02514, respectively by log-rank test) than others. The results of this study show for the first time that overexpression of the HDAC protein is a frequent event in oral cancer and could be used as a prognostic factor in oral SCC. We further investigated the role(s) of HDAC2 in oral carcinogenesis. We found that human oral cancer TW2.6 CC-2, -4, -6 cells with higher invasive ability exihibited higher HDAC2 expression.Recent studies have demonstrated that HDAC inhibitors (HDACIs) possess antitumor activity and are well tolerated, supporting the idea that their use might be a specific strategy for treatment of oral cancer. In this study, we investigate the effect of suberoyl anilide bishydroxamine (SAHA, one of the most potent HDACI) on SAS and Ca9-22. Here, we demonstrated that SAHA induces apoptosis in SAS and Ca9-22 cells as evidenced by PARP cleavage and nuclear DNA fragmentation ELISA. In combination with the clinical findings, the present stady demonstrated that HDAC2 may also play a role in regulating the invasive ability of oral cancer cells.
Subjects
histone deacetylases (HDAC)
Oral squmous cell cancer
SDGs
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