放射治疗是胶质瘤重要治疗手段之一。但是，由于放射抵抗影响了胶质瘤放射治疗的有效性。前期研究显示放射抵抗胶质瘤组织中PGK1高表达；诱导PGK1高表达的胶质瘤细胞中CIN、CFL1显著增加；PGK1与CIN存在相互作用。因此，我们提出：PGK1激活CIN介导胶质瘤放射敏感性降低的新机制。本研究拟通过利用南京医科大学生殖医学国家重点实验室高通量蛋白质组平台，围绕假说开展深入研究：首先应用高分辨质谱技术研究PGK1与CIN相互作用及作用位点，明确PGK1如何对CIN产生作用；其次通过点突变、shRNA等技术在体内外研究PGK1修饰CIN对胶质瘤放射敏感性的影响；应用高通量测序技术分析PGK1修饰CIN后胶质瘤细胞转录组水平变化，更深层次寻找放射敏感性降低原因。通过研究阐明PGK1磷酸化CIN对胶质瘤放射敏感性的影响。该分子机制目前尚未见报道，本研究结果将为提高胶质瘤放射敏感性提供新靶标。

Radiotherapy is one of the most important treatments for glioma. However, radioresistance affects the effectiveness of radiotherapy for glioma. Previous studies showed that PGK1 was highly expressed in radioresistant glioma tissues. CIN and CFL1 were significantly increased in glioma cells induced by high expression of PGK1. There was interaction between PGK1 and CIN. Therefore, we propose that PGK1 activates CIN mediated radiosensitivity reduction in glioma..The study was based on the platform of high-throughput proteome of the National Key Laboratory of Reproductive Medicine of Nanjing Medical University. This study aims to carry out in depth research around hypothesis. Firstly, the interaction between PGK1 and CIN was studied by high resolution mass spectrometry, and how PGK1 acts on CIN was clarified. Secondly, the effect of PGK1 modified CIN on radiosensitivity of glioma was studied in vitro and vivo by methods of point mutation, shRNA et al. High-throughput sequencing was used to analyze the transcriptome changes of glioma cells after PGK1 modified CIN, and to further explore the reasons for the decrease of radiosensitivity. The molecular mechanism of PGK1 phosphorylated CIN on glioma radiosensitivity has not been reported yet. The results of this study will provide a new target for improving radiosensitivity of glioma.