Enolase1(ENO1)是糖酵解过程的限速酶，与肿瘤的发生、发展关系密切，有望成为肿瘤治疗的新靶点。CSP是由海鞘中获得的抗肿瘤多肽，已获重组表达，其对多种肿瘤细胞显示良好的杀伤活性，但对正常细胞却无抑制作用。进一步分析表明CSP能够与ENO1结合，且能显著抑制ENO1高表达细胞的生长和转移，说明ENO1是CSP的直接作用靶点，但尚不明确CSP与ENO1的相互作用机制。本项目以结肠癌细胞为研究对象，拟研究CSP与ENO1结合对ENO1结构与功能的影响、鉴定CSP与ENO1的结合位点，研究CSP拮抗ENO1对结肠癌细胞能量代谢和细胞迁移的影响及可能的影响途径，揭示CSP与ENO1蛋白的相互作用规律、阐明ENO1在肿瘤细胞能量代谢和细胞转移中的调控作用。通过本研究将明确CSP的抗肿瘤作用机制，并对确定ENO1作为新型抗肿瘤靶标及发展新型的海洋抗肿瘤新药都具有重要的科学价值。

Enolase isoform 1(ENO1),a rate-limiting enzyme of glycolytic cycle, plays critical role in tumor genesis and development. ENO1 has a potential to be a novel target in cancer therapy, CSP (Ciona savignyi polypeptide) is a novel anti-tumor ploypeptide isolated from Ciona savignyi. Recent study in our laboratory found that CSP displays potent anticancer activity to several human cancer cells, but the polypeptide shows little sensitivity on normal cells . Further study reveals that the polypeptide could bind with ENO1 specifically, inducing apoptosis in cells expressing high level of ENO1. Our results strongly suggest that ENO1 is the target of CSP in human cancer cell.However,little is known about the mechnism of CSP interacts with ENO1. In the present study, we plan to study the interaction of CSP and ENO1 in human HCT116 cell, identify the CSP binding domain on ENO1. Moreover, we will study the energy metabolism and metastasis of HCT116 cancer cells in the presence of CSP to elucidate the interaction of CSP with ENO1 on cancer cell function as well as the potential signal pathway of CSP on cancer cell energy metabolism and cell metastasis，document the underlining mechanism of interaction between ENO1 and CSP. This study is important for developing ENO1 as a novel target in cancer therapy and also have great vale for developing the marine polypeptide as a novel anticancer agent.