Amplification of Rad9 in head and neck cancer

近年来，越来越多的证据表明，头颈部鳞状细胞癌中存在一种不能通过化疗或放射治疗根除的耐药肿瘤细胞亚群。人RAD9参与细胞周期检查点、DNA损伤修复和细胞凋亡。此前的研究表明，Rad9在头颈癌的上皮性肿瘤细胞中经常被扩增，但对其在头颈癌发生发展中的作用知之甚少。在这里，我们研究了RAD9和P53在调节P21基因表达中的直接联系。免疫组织化学分析显示，在头颈部癌组织中，肿瘤细胞核内有Rad9的聚集，并与p53共存。此外，分子生物学研究揭示了Rad9和Rev7的直接联系，Rev7是一种容易出错的DNA聚合酶。总体而言，这些发现表明hRad9可能在遗传不稳定和癌症发生中发挥作用。进一步的实验可能会揭示其作为诊断和预后因子的作用，并可能作为治疗靶点。

In the recent years, evidence is increasing indicating the existence of a subpopulation of resistant tumor cells in head and neck squamous cell carcinoma that cannot be eradicated by chemotherapy or radiotherapy. Human Rad9 is involved in cell cycle checkpoints, repair of damaged DNA, and apoptosis. Previous studies suggest that Rad9 is frequently amplified in epithelial tumor cells of head and neck cancer, but little is known about its role in the development of head and neck cancer. Here we studied the direct association of Rad9 and p53 results in regulation of the expression of P21 gene. Immunohistochemistrical analysis in head and neck cancer detected the accumulation of Rad9 in the nuclei of tumor cells, which colocalized with p53. In addition, molecular biological studies revealed the direct association of Rad9 and Rev7, an error-prone DNA polymerase. Collectively, these findings suggest that hRad9 may play a role in genetic instability and carcinogenesis. Further experiments might reveal its role as a diagnostic and prognostic factor, and possibly as a therapeutic target.