宫颈癌是最常见的妇科恶性肿瘤，HPV感染是其重要的外在因素，而阐明发病的内在机制意义重大。国内外研究发现：BAP31是内质网转运蛋白，参与内质网稳态维持、细胞凋亡等重要生物过程。课题组前期证实：BAP31作为一种新的肿瘤/睾丸抗原，其表达与宫颈癌发生发展成正相关，影响增殖凋亡及侵袭迁移等细胞行为。我们还发现：BAP31在mRNA和蛋白水平表达不对等提示其在宫颈癌中高表达是转录后调控异常所致；生物信息学及预实验显示miR-362可负调节BAP31表达；临床小样本及分子生物学实验提示宫颈癌中MYC家族转录失能是miR-362下调的重要原因；进一步发现BAP31可与Bip/Grp78形成复合体、兼具ceRNA关系。那么，上述分子构成的调控网络是否为宫颈癌发生的内在推手？本课题拟系统探讨MYC家族、miR-362及BAP31分子网络失调促进宫颈癌发展的内在分子机制，为疾病的防治提供新靶点和新思路。

Cervical cancer is the most common female malignancy. HPV infection is an important extrinsic reason, however, pursuing for the intrinsic mechanism of tumor development is significant. Studies overseas reported that BAP31 is an ER transporter, which engaged in crtical biofunctions such as ER homeostasis and cellular apoptosis. Our previous study found BAP31 a novel cancer/testis antigen, of which expression profile was positively correlated with progression of cervical cancer, and which had effect on cellular behaviors like proliferation, apoptosis, cell cycle, invasion and migration. We also discovered that posttranscription modification should be blamed for the discontinuity expression of BAP31 from mRNA to protein in cervical cancer; miR-362 downregulated BAP31, which was confirmed by bioinformatics and labwork; the loss of transcriptive function of MYC family led to miR-362 low expression in cervical cancer; and bilateral links between BAP31 and Bip/Grp78 were symbolized by ceRNA and protein interaction, which suggested a complicated mechanism in cervical cancer. So, is that the regulation network mentioned above the inner promotion of cervical cancer? This project means to systematically interpret that molecular network dysregulation of MYC family, miR-362 and BAP31 is an inner promotion of cervical cancer, and to put forward new targets and fresh ideas for disease prevention and control.