The role of EVI1 in myeloid malignancies

被引：57

作者：

Glass, Carolyn ^{[1
]}

Wilson, Michael ^{[1
]}

Gonzalez, Ruby ^{[1
]}

Zhang, Yi ^{[1
]}

Perkins, Archibald S. ^{[1
]}

机构：

[1] Univ Rochester, Sch Med, Dept Pathol & Lab Med, Rochester, NY 14642 USA

来源：

BLOOD CELLS MOLECULES AND DISEASES | 2014年 / 53卷 / 1-2期

基金：

美国国家卫生研究院;

关键词：

Leukemogenesis; Oncogenes; EVI1; Myeloid leukemia; Apoptosis; Differentiation; BINDING-PROTEIN EPSILON; ZINC FINGERS; GRANULOCYTIC DIFFERENTIATION; TRANSFORMING GENE; LEUKEMIA; ACTIVATION; TRANSCRIPTION; EXPRESSION; CELLS; PROTOONCOGENE;

D O I：

10.1016/j.bcmd.2014.01.002

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The EVI1 oncogene at human chr 3q26 is rearranged and/or overexpressed in a subset of acute myeloid leukemias and myelodysplasias. The EVI1 protein is a 135 kDa transcriptional regulator with DNA-binding zinc finger domains. Here we provide a critical review of the current state of research into the molecular mechanisms by which this gene plays a role in myeloid malignancies. The major pertinent cellular effects are blocking myeloid differentiation and preventing cellular apoptosis, and several potential mechanisms for these phenomena have been identified. Evidence supports a role for EVI1 in inducing cellular quiescence, and this may contribute to the resistance to chemotherapy seen in patients with neoplasms that overexpress EVI1 Another isoform, MDS1EVI1 (or PRDM3), encoded by the same locus as EVI1, harbors an N-terminal histone methyltransferase(HMT) domain; experimental findings indicate that this protein and its HMT activity are critical for the progression of a subset of AMLs, and this provides a potential target for therapeutic intervention. (C) 2014 Published by Elsevier Inc.

引用

页码：67 / 76

页数：10

共 84 条

[21] EZH2 inhibition: targeting the crossroad of tumor invasion and angiogenesis [J].

Crea, Francesco ;

Fornaro, Lorenzo ;

Bocci, Guido ;

Sun, Lei ;

Farrar, William L. ;

Falcone, Alfredo ;

Danesi, Romano .

CANCER AND METASTASIS REVIEWS, 2012, 31 (3-4) :753-761

[22] Both AML1 and EVI1 oncogenic components are required for the cooperation of AML1/MDS1/EVI1 with BCR/ABL in the induction of acute myelogenous leukemia in mice [J].

Cuenco, GM ;

Ren, RB .

ONCOGENE, 2004, 23 (02) :569-579

[23] Selective Killing of Mixed Lineage Leukemia Cells by a Potent Small-Molecule DOT1L Inhibitor [J].

Daigle, Scott R. ;

Olhava, Edward J. ;

Therkelsen, Carly A. ;

Majer, Christina R. ;

Sneeringer, Christopher J. ;

Song, Jeffrey ;

Johnston, L. Danielle ;

Scott, Margaret Porter ;

Smith, Jesse J. ;

Xiao, Yonghong ;

Jin, Lei ;

Kuntz, Kevin W. ;

Chesworth, Richard ;

Moyer, Mike P. ;

Bernt, Kathrin M. ;

Tseng, Jen-Chieh ;

Kung, Andrew L. ;

Armstrong, Scott A. ;

Copeland, Robert A. ;

Richon, Victoria M. ;

Pollock, Roy M. .

CANCER CELL, 2011, 20 (01) :53-65

[24] A simple FISH assay for the detection of 3q26 rearrangements in myeloid malignancy [J].

De Melo, V. ;

Vetter, M. ;

Mazzullo, H. ;

Howard, J. D. ;

Betts, D. R. ;

Nacheva, E. P. ;

Apperley, J. F. ;

Reid, A. G. .

LEUKEMIA, 2008, 22 (02) :434-437

[25] EVI1-mediated down regulation of MIR449A is essential for the survival of EVI1 positive leukaemic cells [J].

De Weer, An ;

Van der Meulen, Joni ;

Rondou, Pieter ;

Taghon, Tom ;

Konrad, Torsten A. ;

De Preter, Katleen ;

Mestdagh, Pieter ;

Van Maerken, Tom ;

Van Roy, Nadine ;

Jeison, Marta ;

Yaniv, Isaac ;

Cauwelier, Barbara ;

Noens, Lucien ;

Poirel, Helene-Antoine ;

Vandenberghe, Peter ;

Lambert, Frederic ;

De Paepe, Anne ;

Sanchez, Maria Garcia ;

Odero, Maria ;

Verhasselt, Bruno ;

Philippe, Jan ;

Vandesompele, Joke ;

Wieser, Rotraud ;

Dastugue, Nicole ;

Van Vlierberghe, Pieter ;

Poppe, Bruce ;

Speleman, Frank .

BRITISH JOURNAL OF HAEMATOLOGY, 2011, 154 (03) :337-348

[26] 4 OF THE 7 ZINC FINGERS OF THE EVI-1 MYELOID-TRANSFORMING GENE ARE REQUIRED FOR SEQUENCE-SPECIFIC BINDING TO GA(C/T)AAGA(T/C)AAGATAA [J].

DELWEL, R ;

FUNABIKI, T ;

KREIDER, BL ;

MORISHITA, K ;

IHLE, JN .

MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (07) :4291-4300

[27] Methylation and silencing of miRNA-124 by EVI1 and self-renewal exhaustion of hematopoietic stem cells in murine myelodysplastic syndrome [J].

Dickstein, Jerome ;

Senyuk, Vitalyi ;

Premanand, Kavitha ;

Laricchia-Robbio, Leopoldo ;

Xu, Peng ;

Cattaneo, Francesca ;

Fazzina, Raffaella ;

Nucifora, Giuseppina .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2010, 107 (21) :9783-9788

[28] Stem cell gene expression programs influence clinical outcome in human leukemia [J].

Eppert, Kolja ;

Takenaka, Katsuto ;

Lechman, Eric R. ;

Waldron, Levi ;

Nilsson, Bjoern ;

van Galen, Peter ;

Metzeler, Klaus H. ;

Poeppl, Armando ;

Ling, Vicki ;

Beyene, Joseph ;

Canty, Angelo J. ;

Danska, Jayne S. ;

Bohlander, Stefan K. ;

Buske, Christian ;

Minden, Mark D. ;

Golub, Todd R. ;

Jurisica, Igor ;

Ebert, Benjamin L. ;

Dick, John E. .

NATURE MEDICINE, 2011, 17 (09) :1086-U91

[29]

FUNABIKI T, 1994, ONCOGENE, V9, P1575

[30] Global Identification of EVI1 Target Genes in Acute Myeloid Leukemia [J].

Glass, Carolyn ;

Wuertzer, Charles ;

Cui, Xiaohui ;

Bi, Yingtao ;

Davuluri, Ramana ;

Xiao, Ying-Yi ;

Wilson, Michael ;

Owens, Kristina ;

Zhang, Yi ;

Perkins, Archibald .

PLOS ONE, 2013, 8 (06)

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