“Warburg效应”是肿瘤细胞糖代谢的特点，即高水平的糖酵解帮助细胞适应缺氧环境并获得生长优势，抑制糖酵解已成为抗肿瘤领域的新兴技术。接头蛋白P62参与多种信号调控，是反映自噬水平的重要指标。文献显示自噬和糖酵解关系密切，但尚无报道表明P62能直接促进糖酵解。本课题前期研究发现沉默P62能抑制肝癌细胞增殖，降低葡萄糖摄取量和乳酸产量，抑制酵解通路HK、LDH1和Glut1的表达，过表达P62则能提高糖摄取量、乳酸产量和胞内ATP水平。本课题拟在此基础上探讨P62在肝癌细胞糖酵解中的作用及机制：建立稳定沉默和过表达P62的肝癌细胞株，在体外检测P62对细胞生长、糖酵解和有氧呼吸的影响，在体内评估P62对肿瘤生长的影响，探讨P62影响糖酵解的分子机制，寻找与P62相互作用的因子并确认作用位点。通过本课题的研究，明确P62与肿瘤细胞糖酵解之间的关系，为开发糖代谢相关的抗肿瘤药物提供理论依据。

"Warburg effect" is a feature of glycometabolism in tumor cells. High-level glycolysis helps cells to adapt hypoxia and obtain growth advantage. Inhibiting glycolysis has become one of the novel strategies in anti-cancer field. The adaptor protein P62 is involved in regulation of many signaling pathways and is an important index to reflect the autophagy level. Evidence has revealed that there is a close relationship between autophagy and glycolysis, but there has been no evidence indicating that P62 can enhance glycolysis progression directly. Previous research showed that silencing P62 could suppress cell proliferation, reduce glucose uptake and lactate production, and inhibit expression of HK, LDH1 and Glut1 in the glycolysis pathway. P62 over-expression could elevate glucose uptake, lactate production and intracellular ATP level. This program is intended to discuss the effect of P62 on glycolysis and the molecular mechanisms in hepatoma cells on the basis of previous data: It’s to establish hepatoma carcinoma cell lines with long-term silence and over-expression of P62, detect the role of P62 in cell growth, glycolysis and aerobic respiration in vitro, evaluate the effect of P62 on tumor growth in vivo, explore the molecular mechanisms, look for the interacting targets and identify the acting sites. This program will elucidate the relationship between P62 and glycolysis in tumor cells, and provide theoretic basis for development of the glycometabolism-associated anti-tumor medicine.