转移和复发是宫颈癌患者死亡的主要危险因素，故加强宫颈癌侵袭进展机制的基础研究，阐明宫颈癌转移的分子机制，是提高宫颈癌治愈率和降低死亡率的关键。本项目前期研究通过对宫颈癌进行双重RNA-seq发现FAM83A是新的宫颈癌相关分子，随后初步功能研究发现FAM83A表达抑制能够显著增强宫颈癌细胞的迁移和侵袭能力，但对其如何调控宫颈癌细胞的黏附、侵袭和转移仍不清楚。本项目拟通过RNA-seq和细胞功能研究进一步探索FAM83A作为宫颈癌转移抑制因子的具体作用机制，阐明FAM83A表达抑制能够上调多个编码laminin及其受体integrin的基因表达，进而激活PI3K/AKT关键信号通路参与宫颈癌细胞的黏附和侵袭转移，最后通过动物实验及临床组织标本体内验证该调控机制。阐明FAM83A调控宫颈癌转移的崭新机制，将丰富宫颈癌进展理论，为肿瘤转移研究提供新的方向，为开发有效的抗肿瘤临床治疗提供新的思路。

Metastasis and recurrence are the main reason for the death of cervical cancer. Thus, illustrating its underlying mechanism is of great importance. On the basis of our preliminary studies, we conducted two RNA-seqanalyses from 14 different clinical cervical tissues with two sepatate platforms, each containing normal cervical tissues and cervical cancer tissues. We chose FAM83A for further study. We foundFAM83Ainhibition significantly increased the migration and invasion ability of cervical cancer cells. However, the mechanism of FAM83A in cervical cancer metastasis is still unknown. Our study will identify the function role of FAM83A in cervical cancer cells. Then, we will suppress the expression of FAM83A, following RNA-seq to identify the downstream targets, and confirm the main pathwaysregulated by FAM83A. Furthermore, we will explore the relationship between FAM83A, laminin, integrin, PI3K and AKT in clinical cervical cancer tissue samples. Our study is to show FAM83A suppresses lamininand integrin expression, followed by inhibition of PI3K/AKT pathway, and finally suppresses the adhesion, invasion, and metastasis of cervical cancer cells. Classifying the novel mechanism of FAM83A in metastasis of cervical cancer will enrich the theory of cervical cancer progression, provide the new direction for tumor metastasis and the new thinking for developing anti-tumor drugs.