Abstract 4954: The expression of X-linked inhibitor of apoptosis in human oral squamous cell carcinoma and its relationship with clinical factors

Abstract

Abstract [Background] X-linked inhibitor of apoptosis (XIAP) is a member of the inhibitor of apoptosis protein family, which is associated with cell survival by blocking caspase-mediated apoptosis. XIAP is expressed in various malignant tumors. The overexpression of XIAP has been reported to be a poorer prognostic factor in various malignancies. However, the prognostic value of XIAP expression in patients with oral cancer is not still cleared. [Purpose] The aims of present study were to evaluate the expression of XIAP protein in oral squamous cell carcinoma (OSCC) and to elucidate the relationships among the XIAP expression, clinical stages, histological differentiation and classification of invasion mode. [Materials and Methods] Four human OSCC cell lines, B88, CAL27, HNt, and HSC3 cells were used in this study. Normal gingival epithelial cells served as control. XIAP expression of cultured cells was detected by western blot. Tissue specimens were obtains from 85 patients with OSCC after surgery or biopsy. XIAP expression was detected by an immunohistochemical method. [Results] The expression of XIAP was detected in all cancer cells, but not in normal cells. Immunohistochemical analysis of 85 cases of OSCC showed that 73 (86%) cases expressed XIAP. There was no relationship between XIAP expression and clinical stages, or classification of invasion mode. There were significant differences between XIAP expression and histological differentiation. Most of non-staining and weakly staining of cancer was well differentiated. In contrast, intense and extensive staining was frequently found in poorly differentiated cancer. [Conclusions] These findings suggested that the expression of XIAP in OSCC could be related to histological differentiation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4954. doi:1538-7445.AM2012-4954