AML1-ETO相关融合环状RNA通过ENO1调控白血病细胞糖酵解的作用研究

t(8;21)(q22;q22.1)是急性髓系白血病常见的染色体易位改变之一，其形成的AML1-ETO融合蛋白可以阻止造血干祖细胞分化并诱导白血病的发生。环状RNA(CircRNA)是非编码RNA的一种，其可与蛋白或miRNA结合参与肿瘤的发生与发展。我们的前期研究结果验证了AML1-ETO相关的环状RNA(F-CircAE)可以维持白血病细胞的生长，并上调糖酵解的转录组水平。进一步研究发现F-CircAE与糖酵解关键蛋白ENO1结合；但其具体的作用机制尚未做深入的研究。本项目拟验证F-CircAE是否可以与ENO1相互结合；并探索F-CircAE通过ENO1调节糖酵解的具体作用机制。通过上述研究旨在更全面的了解AML1-ETO白血病的发病机制。

The translocation of t(8;21)(q21;q22) is one of the most common chromosomal rearrangements happened in acute myeloid leukemia. The roles of AML1-ETO have been characterized by leading to hematopoietic differentiation blockage and leukemogenesis. CircRNA is one of the noncoding RNAs and mainly function as sponges or decoys for miRNA or proteins in tumor development and progression. Our previous study demonstrated that AML1-ETO related fusion circular RNAs (F-CircAE) contribute to the proliferation of leukemia cells, and the transcripts level of aerobic glycolysis was up-regulated. Further research found that F-CircAE binds to the key glycolysis protein ENO1. However, the mechanism has not been studied in depth. Our work is to uncover the regulatory mechanism of F-CircAE on ENO1 and its function in glycolysis and leukemia progression. Our research attempts to understand the pathogenesis of AML1-ETO leukemia more comprehensively.