酪蛋白激酶FAM20C被报道可参与多种肿瘤的发生过程，但其在胶质瘤中的作用和机制尚不清楚。我们前期发现FAM20C在胶质瘤组织中表达高于正常脑组织，干扰FAM20C可抑制胶质瘤细胞生长和迁移；生物信息学分析发现FAM20C可能磷酸化FN1 S2475位点，预实验结果显示FAM20C与FN1在胶质瘤细胞中存在共定位，干扰FAM20C可抑制FN1磷酸化及其下游FAK/PI3K/AKT信号通路。由此，我们提出假说：FAM20C可直接影响FN1蛋白S2475位点的磷酸化，影响FN1与细胞膜上整合素分子的结合，进而激活FAK/PI3K/AKT信号通路，促进胶质瘤的发生发展。本项目拟从分子、细胞、组织和动物等层面，明确FAM20C与磷酸化FN1在胶质瘤生长和转移中的作用，阐明FAM20C与FN1的调控关系及机制，为胶质瘤的预后评估提供新指标，亦为发展胶质瘤新的治疗靶标奠定基础。

The casein kinase FAM20C has been reported to play critical roles in the progression of various tumors. However, the role and mechanism of FAM20C in glioma remains largely unknown. We previously found that FAM20C was frequently up-regulated in glioma tissues compared with normal brain tissues. Knockdown of FAM20C inhibited cell growth and migration in glioma. Moreover, bioinformatic analysis revealed that FAM20C was possible to regulate the phosphorylation of FN1 (S2475). In our data, co-localization of FAM20C and FN1 was observed in glioma cells by immunofluorescence. Suppression of FAM20C inhibited the phosphorylation of FN1 and its downstream FAK/PI3K/AKT signaling pathway. Thus, we hypothesized that FAM20C directly regulate the phosphorylation of FN1 (S2475), activating the FAK/PI3K/AKT signaling pathway, thus promoting tumor growth and metastasis. To prove this hypothesis, we intend to investigate the role of FAM20C and phosphorylated FN1 on tumor growth and metastasis, clarify the relationship and regulatory mechanism between FAM20C and FN1through experiments in molecular, cellular, tissue and animal. Through our study, we hope to provide novel potential biomarkers for glioma prognosis, and also lay the foundation for developing new therapeutic targets for glioma.