促癌因子通过细胞的核浆信息交换，导致原癌基因或抑癌基因等大分子亚细胞定位异常，从而促进肿瘤的发生发展。因此，针对性阻断肿瘤细胞核浆信号转运过程中的关键载体—核转运蛋白，有望成为治疗肿瘤的突破点。我们前期研究发现核转运蛋白IPO7在宫颈癌中表达显著升高，是宫颈癌预后的不良因素。体内外实验表明，抑制IPO7表达可明显抑制宫颈癌细胞的增殖及成瘤能力，促进细胞的凋亡。进一步提取胞核胞浆蛋白进行蛋白质谱检测并结合生物信息学分析，发现IPO7高表达主要涉及调节mRNA结合蛋白MSI2的转运过程，进而促进宫颈癌的发生发展。本项目拟在前期研究的基础上，采用多种实验技术明确IPO7通过何种机制转运MSI2入核并致使宫颈癌的演进，并筛选IPO7小分子抑制剂或功能性阻断抗体探索靶向IPO7治疗宫颈癌的可能性，从靶向核转运蛋白这一新视角为宫颈癌的防治提供实验基础及理论支持。

Malfunction of nuclear-cytoplasmic transport contributes to the changes of tumor suppressors, oncogenes in both the expression levels and temporal-spatial location，which promotes tumorigenesis and progression. Therefore, blocking the nuclear transporters-karyopherin is expected to be a breakthrough in the therapy of tumors. Our previous study demonstrated that the expression of Importin7(IPO7) was significantly overexpressed in cervical cancer, which was associated with unfavorable survival and was one of adverse prognosis factors in cervical cancer. Knockdown the expression of IPO7 can significantly inhibit the growth and induce apoptosis of cervical cancer cells in vivo and in vitro. Furthermore, the protein mass spectrometry was utilized to analysis the isolated nuclear and cytoplasmic protein when knocked down the expression of IPO7. Combined with bioinformatics analysis, we speculated an RNA binding protein MSI2 may nuclear transported by IPO7 in the progression of cervical cancer. Based on the previous studies, we attempt to clarify the potential mechanism by which IPO7 regulates MSI2 transporting into the nucleus. And to explore the possibility of targeting IPO7 in the treatment of cervical cancer by screening IPO7 small molecule inhibitors or blocking antibodies. In conclusion, our research can provide theoretical support for the new perspective of targeting nuclear-cytoplasmic transporters in the treatment of cervical cancer.