胶质母细胞瘤（GBM）恶性程度高、预后差，其中异柠檬酸脱氢酶1（IDH1）突变型GBM预后好于野生型，但机制不明。预实验证实IDH1突变型中糖代谢关键酶谷氨酸草酰乙酸转氨酶1（GOT1）表达高于野生型，高表达GOT1的IDH1突变型GBM生存时间长、细胞增殖慢，提示IDH1突变型GBM中GOT1高表达抑制肿瘤细胞糖代谢和增殖，后还发现circ-GOT1.4可通过竞争性内源RNA（ceRNA）机制调控GOT1，且其表达在IDH1突变型较高。由此我们提出IDH1突变型中高表达的circ-GOT1.4通过ceRNA上调GOT1，抑制肿瘤糖代谢和增殖，造成突变型预后优于野生型的假说。本课题拟以IDH1突变型和野生型GBM细胞为对象，通过体内外实验对GOT1影响GBM糖代谢与其受circ-GOT1.4调控的机制进行研究，揭示IDH1突变型和野生型GBM预后差异原因，为临床辅助治疗提供新思路和靶点。

Glioblastoma multiforme (GBM) has high malignancy and poor prognosis. GBM with mutant isocitrate dehydrogenase 1 (IDH1) has been found to have a better prognosis than with wild-type, but the mechanism is unclear. Bioinformatic analysis indicated that the expression of glutamate oxaloacetate transaminase 1 (GOT1), the key enzyme of glycometabolism in IDH1 mutant GBM was higher than that in IDH1 wild-type GBM, and the survival time of IDH1 mutant GBM with high expression of GOT1 was longer and cell proliferation was slower. It suggested that the high expression of GOT1 in IDH1 mutant GBM inhibited the glycometabolism and proliferation of GBM cells. Further analysis showed that circ-GOT1.4 could regulate GOT1 through competitive endogenous RNA (ceRNA) mechanism. Preliminary experiments confirmed that circ-GOT1.4 was over-expressed in IDH1 mutant GBM than in IDH1 wild-type GBM. Therefore, we propose the hypothesis that circ-GOT1.4, which is highly expressed in IDH1 mutant GBM, can up-regulate GOT1 by ceRNA, inhibit the glycometabolism and proliferation of GBM cells, and result in a better prognosis of mutant than that of wild type. In this study, we will take IDH1 mutant GBM cells and wild-type GBM cells as objects to study the mechanism of GOT1 affecting GBM glycometabolism and its regulation by circ-GOT1.4 in vivo and in vitro. We will reveal the reasons for the difference of prognosis between IDH1 mutant and wild-type GBM cells, and provide new ideas and targets for clinical adjuvant therapy.