已证实HPV与癌基因DEK mRNA转录密切相关，在宫颈癌发生发展中有重要作用，但其机制尚不清楚。我们前期研究发现：同源盒基因蛋白Six1及其下游细胞粘附蛋白Ezrin可通过促进上皮-间质转化（EMT）导致宫颈癌转移；免疫双荧光研究发现DEK-Six1/Ezrin共同过表达于癌细胞内，提示DEK可能通过调节Six1/Ezrin蛋白表达促进肿瘤发生。本研究拟应用蛋白表达分析和芯片检测等技术，探讨DEK基因和Six1/Ezrin信号通路间的基因表达调控关系，明确其作为宫颈癌诊断及预后评估标志物的价值；体外应用RNAi技术特异性沉默宫颈癌细胞DEK表达，分析其对Six1/Ezrin信号通路基因表达及侵袭能力的影响；建立裸鼠宫颈癌模型，证实DEK通过上调Six1/Ezrin信号通路引发EMT导致肿瘤演进。本研究将阐明DEK促进宫颈癌发生及转移的分子调控机制，可为宫颈癌提供新的肿瘤标志物及治疗靶点。

It has been proved that HPV is highly related with the mRNA transcription of proto-oncogene DEK, and it plays an important role in the occurrence and development of uterine cervical cancers, however, the molecular mechanism is still unclear. We previously found that homeobox gene Six1 and its downstream cell adhesion protein Ezrin are overexpressed in cervical cancer cells, and it can lead to metastasis of cervical cancer by promoting epithelial-mesenchymal transition (EMT); DEK- Six1/Ezrin co-expression are also found by immune double fluorescence staining in cervical cancer cells, suggesting that DEK may promote the progress of cervical cancer by regulating the protein expression of Six1/Ezrin. This study intends to confirm the biomarker value of DEK and Six1/Ezrin on evaluation of cervical cancer diagnosis and prognosis by using gene chip and protein expression detection combined with the detailed clinical data analysis, to analyze the effects and mechanism of DEK on regulation of Six1/Ezrin by silencing DEK expression in cervical cancer cell lines via RNAi technique, and to establish the nude mice tumor model bearing cervical cancer cells for confirming the effects of DEK on the tumorigenesis and EMT of cervical cancers and the regulation mechanism of gene expression. This study will elucidate the molecular regulating mechanism of DEK on promoting the tumorigenesis and metastasis, and provide new tumor markers and therapeutic targets for cervical cancers.