直肠癌是一种常见的恶性肿瘤，在我国的发生率逐年上升。放疗是中、晚期直肠癌治疗常用的方法之一，尽管能够提高局部控制率，但仍不能达到令人满意的治疗效果。由于放疗是通过损伤肿瘤细胞DNA达到治疗目的，并且根据放射生物学发现放疗的核心是放射敏感性。因此，本项目将重点研究DNA损伤修复因子PBK/TOPK对直肠癌放疗敏感性的影响和作用机理，探讨直肠癌放疗敏感组和放疗抵抗组中直肠癌病理组织标本中PBK/TOPK的表达水平与放射敏感性之间的关系，研究沉默PBK/TOPK的直肠癌细胞株给予放射线照射后，PBK/TOPK对直肠癌细胞增殖的影响，并应用裸鼠成瘤模型进一步证实给予放疗后PBK/TOPK对直肠癌细胞增殖的改变，同时将检测沉默PBK/TOPK直肠癌细胞放疗后凋亡因子的变化，最终明确直肠癌放疗中PBK/TOPK如何影放射敏感性，为直肠癌放疗的发展提供新的研究资料。

Rectal carcinoma is a common malignant tumor in the world, the incidence rate and mortality of rectal carcinoma is increasing in China. Radiotherapy is one of the methods used in advanced rectal carcinoma. Although it could improve local control in rectal carcinoma, it do not achieve a good result for patients. Because the mechanism of radiotherapy is to damage DNA of tumor cells. It found that the core problem of radiotherapy is radiation sensitivity. Therefore, this project will be focused on the study for PBK/TOPK, which is DNA damage repair factor, play an important role for radiation sensitivity in rectal carcinoma. To make clear the function mechanism between PBK/TOPK and radiation sensitivity in rectal carcinoma, we will analyze the relationship between PBK/TOPK expression level and radiation sensitivity in two groups of patients of rectal carcinoma, including sensitive to radiation group and radiation resistance group, using immunochemistry. siRNA is using to silence PBK/TOPK in the rectal carcinoma cell lines, which will be examined proliferation after exposed in radiotherapy. The nude mouse tumor model will be applied is to confirm the proliferation of rectal carcinoma cell is decreasing with silencing PBK/TOPK after radiotherapy. To illustrate the mechanism of PBK/TOPK with radiation sensitivity in rectal carcinoma, we will test the apoptotic factor in cell lines and animal tissue. The study will prove the role of PBK/TOPK with radiation sensitivity in rectal carcinoma, and provide new research data for radiotherapy in rectal carcinoma..