Analysis of abnormal DNA structure and down regulation of a new tumor suppressor, FEZ1 gene, in oral squamous cell carcinoma.

8号染色体短臂（8 p）上的等位基因缺失是包括口腔癌在内的几种人类恶性肿瘤的常见事件。我们在口腔鳞状细胞癌（SCC）中发现了两个常见的8 p缺失区（8 p12，8 p22）。此外，还对定位于8 p22的候选肿瘤抑制基因FEZ 1/LZTS 1（FEZ 1）的可能参与进行了评估。在此我们分析了FEZ 1的改变是否在口腔SCC的发生和发展中起作用。在本研究中，我们检测FEZ 1在31个原发性口腔SCC和8 SCC衍生细胞系的表达通过逆转录-PCR（RT-PCR）。35%的肿瘤（31例中的11例）和100%的细胞系（8例中的8例）显示mRNA基因表达缺失或降低。此外，为了研究沉默的机制，将细胞与5-氮杂-2 '-脱氧胞苷一起培养，所有细胞系都显示出去甲基化剂的恢复。这些发现表明，FEZ 1基因的失活可能有助于口腔SCC的发展。

Allelic deletions on the short arm of chromosome 8 (8p) are frequent events inseveral human malignancies, including oral cancer. We have examined and found two common regions of deletion on 8p (8pl2, 8p22) in oral squamous cell carcinomas (SCC) s. The possible involvement of FEZl/LZTSl (FEZ1) gene, a candidate tumor suppressor gene, mapped at 8p22, was also evaluated. Here we analyzed whether FEZl alterations play arole in the development and progression of oral SCCs. In present study, we examined FEZ1 expression in 31 primary oral SCCs and 8 SCC-derived cell line by reverse transcription-PCR (RT-PCR). Thirty-five % of tumor (ll of 31) and 100% of cell lines (8 of 8) showed absent or reduced mRNA gene expression. Furthermore, to investigate the mechanism for silencing, cell were cultured with 5-aza-2'-deoxycytidine and all of cell linesshowed restoration by demethylating agent. These findings suggest that inactivation of the FEZ1 gene may contribute to the development of oral SCCs.