能量代谢在肿瘤发生发展中起重要作用，但肝癌中能量代谢的研究还较欠缺。我们前期已揭示了alpha B-Crystallin（Cryab）过表达诱导肝癌上皮间质转化(EMT)及sorafenib耐药，促进侵袭转移。而肿瘤侵袭转移过程中需要糖类供能。故我们推测Cryab不仅诱导EMT，而且可调节能量代谢。为了证实以上假设，本项目拟检测Cryab诱导EMT过程中及随后Cryab下调诱导间质上皮转化过程中糖类代谢变化；利用表达谱芯片技术结合生物信息学分析并找到Cryab调控糖代谢关键蛋白，采用糖代谢关键蛋白基因转染和干扰技术，双向调节Cryab调控的糖代谢关键蛋白的表达水平，观察细胞侵袭、转移及形态等生物学行为变化调查Cryab调控的能量代谢与EMT关系，并且在肝癌组织及肝癌原位模型验证筛选蛋白与EMT、代谢的关系。而且我们进一步调查筛选蛋白调节的能量代谢能否影响sorafenib耐药。

Energy metabolism plays a critical role in cancers, However, a systematic study for the role of energy metabolism in hepatocellular carcinoma is lacked. Previously, we detected alpha B-Crystallin (Cryab) overexpression induced epithelial-mesenchymal transition (EMT), promoting liver cancer cell invasion and metastasis. The process of tumor invasion and metastasis needs glucose for energy. Therefore, we hypothesized that Cryab not only induce EMT, and may regulate energy metabolism. To confirm these assumptions, the study intends to investigate glucose metabolic changes during Cryab-induced EMT process and subsequent epithelial mesenchymal transformation process by Cryab down-regulation. Using Gene microarray technology can detect Cryab-regulated genome-wide distribution patterns, and then we combine the data with bioinformatics analysis and find key protein regulating glucose metabolism. Using gene transfection regulates the level of key protein, changes of cell invasion, metastasis biological behavior and morphology are observed, while the relationship between the key protein and EMT, metabolism is investigated in orthotopic liver cancer model. Moreover，we investigated the relationship between the energy metabolism the above key protein regulated and sorafenib resistance.