E2-2, a member of the E protein family, is able to influence the function of the AETFC composite.

On December 28, 2018, the International Academic Journal of the National Academy of Sciences (PNAS) published online the collaboration paper "Differents of the University of Science and The E Proteins in t (8;21)" by Wang Lan Research Group of the Shanghai Institute of Nutrition and Health of the Chinese Academy of Sciences and Sun Xiaojian Research Group of Ruijin Hospital, affiliated with Shanghai Jiaotong University, and Robert G. Roeder of Rockefeller University in the United States. E2-2-turn-the-function of the function of the function of the function a negatively regulates the regulations leukemogenesis", the study found that E protein family members E2-2 can be able to influence the AETFC (AML1-ETO-containing physio) composite function thus negative regulation AML1-ETO fusion protein-induced t (8;21) The occurrence of acute myeloid leukemia.
the disease-causing fusion protein AML1-ETO plays a vital role in the development of t (8:21) leukemia, aML1-ETO in leukemia cells as a stable protein complex exists and functions, the researchers named this complex AETFC.
AETFC's member proteins HEB and E2A belong to the E protein family and are important for the occurrence of AML1-ETO-mediated t (8;21) leukemia.
interestingly, the researchers found that E2-2, the third member of the E protein, was not expressed in t (8;21) leukemia cells, suggesting that E2-2 may be a negative regulatory factor for t (8;21) leukemia.
therefore, the study of the role and mechanism of E2-2 in the occurrence of leukemia can further deepen the understanding of the pathogenesis of leukemia, and has important guiding significance for the clinical diagnosis and treatment of leukemia.
studies have found that overexpression of E2-2 can specifically inhibit the growth of Kasumi-1 cells carrying the AML1-ETO fusion gene, and that the effect is dependent on the BHLH (basic helix-loop-helix) domain of E2-2.
analyzed Kasumi-1 cells in RNA-seq and ChIP-seq and found that E2-2 can transfer AETFC to new target genes, activate genes associated with cell differentiation, such as THPO, and induce leukemia cells to differentiate into dendritic cells.
in leukemia patient syllamy specimens, the expression of E2-2 was relatively low in M2b subtypes, and the expression level of the target gene THPO of E2-2 was correlated with the recurrence rate of patients;
these results suggest that E2-2 may form a new AETFC subtype that acts as a negative regulatory factor for t (8:21) leukemia by regulating the AETFC heterogeneity.
Liu Na, a 2015 ph.d. student at Shanghai Institute of Nutrition and Health, Song Junhong, chief physician of Shanghai Children's Medical Center, and Xie Yangyang, a doctoral student, are the co-first authors.
the study was supported by Chen Saixuan, a member of the Chinese Academy of Engineering at Ruijin Hospital, affiliated with Shanghai Jiaotong University School of Medicine, Chen Qi, a member of the Chinese Academy of Sciences, Stephen Nimer, a professor at the University of Miami School of Medicine, Dr. Shen Shuhong, director of the Shanghai Children's Medical Center, Dr. Lan Fei, Professor of Shanghai Medical School at Fudan University, Zhang Qunling, Director of The Oncology Hospital of Fudan University, and Gao Feifei, A.
the research was supported by the Ministry of Science and Technology's National Key Research and Development Program, the National Natural Science Foundation of China, the Scientific Research Fund of the Chinese Academy of Sciences, the National Key Laboratory of Medical Genomics, etc., as well as the public technology platform of the Shanghai Institute of Nutrition and Health and the support of the animal platform.
Source: Shanghai Institute of Nutrition and Health.