恶性肿瘤生长和增殖迅速，需要充足的营养物质和能量供给。肿瘤细胞代谢出现明显改变以适应肿瘤的发生和发展，其主要表现为：葡萄糖有氧酵解代谢，脂类和核苷酸生物合成增强，肿瘤代谢特征已经成为新的肿瘤恶性表型。肿瘤代谢异常与癌基因MYC 的活化与抑癌基因P53的失活密切相关，但是其具体分子机制尚未阐明。本课题组克隆的抑癌基因 NDRG2是转录因子Myc和p53的靶基因，能够抑制肿瘤细胞糖酵解代谢产物乳酸的产生和葡萄糖的消耗。在此基础上，本课题：首先明确NDRG2在肿瘤代谢中的作用，分析NDRG2调控肿瘤代谢途径和靶点；然后分析NDRG2在Myc诱导的肿瘤细胞有氧酵解和谷氨酰胺分解代谢中的作用；最后探索NDRG2在p53抑制肿瘤代谢恶性表型中的作用。本研究不仅为深入理解NDRG2抑制肿瘤发生和发展的分子机制，而且期望发现新的调控肿瘤代谢靶点，为肿瘤治疗提供线索。

Malignant tumor grow and proliferate rapidly, which need plenty of nutrients and energy supply. Tumor metabolism changes significantly to adapt to tumor occurrence and development, and the characteristics of tumor metabolism are follows: glucose aerobic glycolysis, enhanced lipid and nucleotide biosynthesis, and these tumor metabolic characteristics become the new malignant phenotype. The metabolic derangements in cancer cells may arise from aberrant signaling due to oncogene activation such as MYC, and tumor suppressor gene inactivation such as p53. However, the mechanisms of p53 and Myc signaling drive cancer metabolism reprogramming remains unclear. The tumor suppressor gene NDRG2, which is cloned by our research group, is the target gene regulated by Myc and p53. In addition, NDRG2 inhibits lactic acid accumulation and glucose consumption in tumor glycolysis. On this basis, we prefer to firstly clarify the function of NDRG2 in tumor metabolism, analyze the metabolic pathway and target regulated by NDRG2; Secondly, to analyze the role of NDRG2 in Myc-induced tumor aerobic glycolysis and glutamine catabolism; Finally, to explore the the role of NDRG2 in p53 inhibition in the malignant phenotype of tumor metabolism. Our study will not only further understand the molecular mechanisms of NDRG2 inhibition of tumorigenesis and development, but also expect to discover new Ndrg2-related metabolic targets, and provide clues for the prevention and treatment of malignant tumor.