TARP在牙源性角化囊性瘤发病机制中的作用研究

T-cell receptor gamma chain alternative reading frame protein (TARP) has recently been proposed as the potential diagnosed marker for breast and prostate cancer, which means it has important effect in the occurrence and progression of tumor. And our previous researches found that the copy number of TARP loci amplificated in the epithelial of KCOTs by SNP 6.0 microarray scanning, and the intense immunoreactivity for TARP was detected in KCOTs with specific location in the epithelial cells while absent in the fibro cyst wall of KCOTs and the epithelial cells of normal mucosas. The high expression of TARP on the epithelial cells of KCOTs suggested that it possibly plays a significant role in the pathogenesis of KCOTs and it may be caused by the amplification of copy number. Therefore, we will explore the role of TARP in the molecular pathogenesis of KCOTs in this study through the RNA interference, microarray and so on.

TARP是T细胞受体γ链改变阅读框蛋白，作为潜在的前列腺癌和乳腺癌的标志物，其在肿瘤的发生或发展中有着重要的作用。我们的前期研究在用SNP6.0芯片筛选牙源性角化囊性瘤新的致病基因时发现，牙源性角化囊性瘤的上皮组织中，TARP基因所在的区域有拷贝数增加的现象，并且免疫组化也证实其在牙源性角化囊性瘤的上皮组织中特异性高表达，而在纤维囊壁组织以及正常粘膜中均未检测到；提示TARP在牙源性角化囊性瘤发生发展中可能起到重要的调控作用。因此，本研究将通过显微切割、RNAi及蛋白芯片等技术，探讨TARP在牙源性角化囊性瘤发病中可能的作用及机制，有望揭示牙源性角化囊性瘤发病的新的分子机制。

TARP是T细胞受体γ链改变阅读框蛋白，作为潜在的前列腺癌和乳腺癌的标志物，其在肿瘤的发生或发展中有着重要的作用。我们的前期研究在用SNP6.0芯片筛选牙源性角化囊性瘤新的致病基因时发现，牙源性角化囊性瘤的上皮组织中，TARP基因所在的区域有拷贝数增加的现象，并且免疫组化也证实其在牙源性角化囊性瘤的上皮组织中特异性高表达，而在纤维囊壁组织以及正常粘膜中均未检测到；提示TARP在牙源性角化囊性瘤发生发展中可能起到重要的调控作用。因此，本研究显示，TARP 在正常口腔黏膜上皮细胞系HIEOC并未表达，通过构建TARP慢病毒过表达载体转染HIOEC后，其增殖和迁移能力增强，提示TARP可能通过该方式影响疾病的发生。表达谱芯片也显示，TARP过表达后，与肿瘤信号同路相关的一些基因出现了有差异的变化。该研究结果为了解新的KCOTs发病机制提供了可能的研究方向。