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To explore the expression of X-linked inhibitor of apoptosis protein (XIAP) in Tca8113 cell, and to investigate its relationship to the chemoresistance. METHODS; The Tca8113 cell line was cultured by IMDM and the concentration of Pingyangmycin (PYM) added to Tca8113 cell line was increased gradually and continually, which was to induce the PYM-resistance in Tca8113 cell line. The sensitivity of Tca8113 cell to PYM and expression of XIAP were measured with methyl thiazolyl tetrazolium (MTT) chromatometry and reverse transcription-polymerase chain raction (RT-PCR). The XIAP level in the cells and its chemoresistance to PYM were analyzed by linear regression.The IC50 of Tca8113-1-10 group and Tca8113-10-10 group were(12.758 +/- 0.030), (18.986 +/- 0.150) microg x mL(-1) respectively. The IC50 of Tca8113-1-20 group and Tca8113-10-20 group increased to (26.302 +/- 0.072), (35.294 +/- 0.115) microg x mL(-1) respectively. There was a relation between XIAP and the drug-resistance in Tca8113 cell.XIAP may play an important role in the chemoresistance which might serve as a new therapeutic target for oral squamous cell carcinoma.

To clarify expression and subcellular localization of XIAP and XAF1 protein in human normal oral keratinocytes (hNOK) and Tca8113 cells human tongue carcinoma cell line.The hNOKs and Tca8113 cells were cultured in vitro. Expression and subcellular localization of XIAP and XAF1 protein were examined by combination of indirect immunofluorescence and confocal laser scanning microscopy.XIAP expression was weak in the hNOKs and fluorescence staining localized chiefly in the cytoplasm and perinuclear areas. In the Tca8113 cells, high level of XIAP protein could be detected in both the cytoplasm and the nucleus. In the hNOKs, XAF1 distributed mostly in the nucleus. Homogeneous nuclear and cytoplasmic distribution of XAF1 could be visualized in the Tca8113 cells.In cancerization of oral mucosa, XIAP protein could play an important antiapoptotic role by overexpression, while XAF1 protein does not appear to antagonize effectively the role of XIAP.