Evi1 forms a bridge between the epigenetic machinery and signaling pathways

被引:30
作者
Yoshimi, Akihide [1 ]
Kurokawa, Mineo [1 ]
机构
[1] Univ Tokyo, Dept Hematol & Oncol, Grad Sch Med, Tokyo, Japan
基金
日本学术振兴会;
关键词
Evi1; Leukemia; Polycomb; PTEN; Rapamycin; ACUTE MYELOID-LEUKEMIA; HOST-DISEASE PROPHYLAXIS; HEMATOPOIETIC STEM-CELLS; COMPARATIVE GENOMIC HYBRIDIZATION; METHYLTRANSFERASE GENE EZH2; HISTONE METHYLTRANSFERASE; SOMATIC MUTATIONS; PHOSPHOINOSITIDE; 3-KINASE/AKT; CONTROLS PROLIFERATION; JAK/STAT PATHWAYS;
D O I
10.18632/oncotarget.304
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Recent studies have demonstrated the significance of the leukemia oncogene Evi1 as the regulator of hematopoietic stem cells and marker of poor clinical outcomes in myeloid malignancies. Evi1-mediated leukemogenic activities include a wide array of functions such as the induction of epigenetic modifications, transcriptional control, and regulation of signaling pathways. We have recently succeeded in comprehensively elucidating the oncogenic function of Evi1 in a model of the polycomb-Evi1-PTEN/AKT/mTOR axis. These results may provide us with novel therapeutic approaches to conquer the poor prognosis associated with Evi1-activated leukemia or other solid tumors with high Evi1 expression. Here, we review the current understanding of the role of Evi1 in controlling the development of leukemia and highlight potential modalities for targeting factors involved in Evi1-regulated signaling.
引用
收藏
页码:575 / 586
页数:12
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