靶向肿瘤能量代谢治疗具有潜在的临床意义。有氧糖酵解是肿瘤细胞能量代谢的特征。课题组发现高迁移率族蛋白A1（HMGA1）在肺腺癌高表达,下调HMGA1可抑制糖酵解，但其调控肺腺癌糖酵解的上游机制尚不明确。竞争性内源RNA（ceRNA）网络是指环状RNA（circRNA）与靶基因竞争性结合共同的微小RNA（microRNA）进而发挥生物学作用，但其在糖酵解中的功能尚不清楚。课题组应用生物信息学发现FADS2（circRNA）与let-7a-5p（microRNA）、let-7a-5p与HMGA1靶向结合，其调控作用对肺腺癌糖酵解的影响亟待探明。课题组拟研究肺腺癌FADS2、let-7a-5p和HMGA1与糖酵解的相关性及临床意义，细胞水平明确FADS2作为ceRNA调控HMGA1参与肺腺癌糖酵解的机制，利用18F-FDG Micro-PET显像在体行分子影像学评价，为靶向肺腺癌治疗提供新靶点。

Targeting tumor energy has potentially clinical significance for oncotherapy. Aerobic glycolysis is one of characteristics of tumor cell energy metabolism. Our studies indicated that high mobility group protein A1 (HMGA1) is up-regulated in lung adenocarcinoma (LUAD) and down-regulation of HMGA1 can inhibit glycolysis process, but its upstream mechanism involved in glycolysis of LUAD is still undefined. Competitive endogenous RNA (ceRNA) network refers to the mechanism that circular RNA (circRNA) regulates biological process by binding to identical microRNA, but its function in tumor glycolysis remains unclear. There are targeted relationships between FADS2 (circRNA) and let-7a-5p (microRNA) , let-7a-5p and HMGA1 found by bioinformatics analysis while its regulation effect on the glycolysis of LUAD needs to be proved urgently. The objective of this study is to assess the correlation and clinical significance of FADS2, let-7a-5p and HMGA1 in glycolysis of LUAD and verify the mechanism how FADS2 acts as ceRNA to regulate HMGA1 in vitro. In addition, 18F-FDG Micro-PET imaging is used to evaluate and confirm the effect of the molecular imaging in vivo, which provides new targets and innovative strategies for the diagnosis and treatment of LUAD.