宫颈癌是新疆妇女恶性肿瘤高发地区之一。以往的研究首次证明，自噬基因emc6在宫颈癌中的表达下降。因此，推测EMC6的低表达可诱导Beclin1依赖性自噬减少或凋亡减少，从而促进宫颈癌的发生。因此，本研究拟采用WB, IF,IHC 及其他方法，验证EMC6对宫颈癌细胞系-裸鼠个体水平宫颈癌细胞生长的抑制作用。在此基础上，进一步进行了LSCFM、GST-pull down、自噬通量等实验，通过Beclin1检测EMC6的过度表达，诱导宫颈癌细胞自噬，促进caspase 3从Beclin1分裂形成Beclin1-c碎片，诱导线粒体细胞毒素C释放，启动肿瘤细胞凋亡，证实EMC6和Beclin1通过调节相互作用改变自噬和凋亡水平，从而影响宫颈癌的发生，为研究宫颈癌的发病机制提供新的线索。这将为今后宫颈癌靶向联合治疗的研究提供新的思路。

Cervical cancer is one of the high incidence of malignant tumors in Xinjiang women. Previous studies have demonstrated for the first time that there is a decrease in the expression of autophagy gene EMC6 in cervical cancer. Therefore,it is speculated that low expression of EMC6 induces the decrease of Beclin1-dependent autophagy or the reduction of apoptosis, which promotes the occurrence of cervical cancer. Therefore, this study intends to use WB, IF,IHC and other methods to verify that EMC6 can inhibit the growth of cervical cancer cells in HeLa cell lines-nude mice-individual levels. On this basis, further experiments such as LSCFM, GST-pull down, and autophagy Flux were performed to detect overexpression of EMC6 through Beclin1 to induce autophagy in cervical cancer cells, and to promote the cleavage of caspase 3 from Beclin1 to form Beclin1-Cfragments. Induces mitochondrial cytotoxin C release, initiates apoptosis of tumorcells, and confirms that EMC6 and Beclin1 alter autophagy and apoptosis levels by regulating their interactions, thereby affecting the occurrence of cervical cancer and providing new clues for improving the pathogenesis of cervical cancer. This will provide new ideas for future research on targeted combination therapy for cervical cancer.