The role of Fli-1 in normal cell function and malignant transformation

被引:101
作者
Truong, AHL
Ben-David, Y
机构
[1] Sunnybrook & Womens Coll Hlth Sci Ctr, Div Canc Biol Res, Toronto, ON M4N 3M5, Canada
[2] TSRCC, Toronto, ON M4N 3M5, Canada
[3] Univ Toronto, Dept Med Biophys, Toronto, ON M5G 2M9, Canada
基金
英国医学研究理事会;
关键词
Fli-1; transcription factor; gene regulation; cancer;
D O I
10.1038/sj.onc.1204042
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Aberrant expression of the Fli-1 transcription factor following genetic mutation has been recognized as a seminal event in the initiation of certain types of malignant transformation. Indeed, the etiology of a number of virally induced leukemias, including Friend virus-induced erythroleukemia, has been associated with Fli-1 overexpression, The clinical relevance of Fli-1 becomes apparent in human Ewing's sarcoma in which Fli-1 is the target of a characteristic chromosomal translocation, As such, Fli-1 has generated considerable interest over the past several years for its role in malignant transformation and tumor progression. This review will present a synopsis of the current research on Fli-1 with emphasis on its function in malignant transformation. Moreover, the possible role of Fli-1 in cellular proliferation, differentiation and survival, as well as the recent development of transgenic and knock-out mice to investigate the function of Fli-1 will be discussed. Finally, the significance of identifying target genes that are regulated by Fli-1 and their role in cellular function will be reviewed.
引用
收藏
页码:6482 / 6489
页数:8
相关论文
共 70 条
[1]   EWS/FLI1 up regulates mE2-C, a cyclin-selective ubiquitin conjugating enzyme involved in cyclin B destruction [J].
Arvand, A ;
Bastians, H ;
Welford, SM ;
Thompson, AD ;
Ruderman, JV ;
Denny, CT .
ONCOGENE, 1998, 17 (16) :2039-2045
[2]   FLI-1 is a suppressor of erythroid differentiation in human hematopoietic cells [J].
Athanasiou, M ;
Mavrothalassitis, G ;
Sun-Hoffman, L ;
Blair, DG .
LEUKEMIA, 2000, 14 (03) :439-445
[3]  
Athanasiou M, 1996, CELL GROWTH DIFFER, V7, P1525
[4]   DNA-BINDING AND TRANSCRIPTIONAL ACTIVATION PROPERTIES OF THE EWS-FLI-1 FUSION PROTEIN RESULTING FROM THE T(1122) TRANSLOCATION IN EWING SARCOMA [J].
BAILLY, RA ;
BOSSELUT, R ;
ZUCMAN, J ;
CORMIER, F ;
DELATTRE, O ;
ROUSSEL, M ;
THOMAS, G ;
GHYSDAEL, J .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (05) :3230-3241
[5]   The GATA-1 and Spi-1 transcriptional factors bind to a GATA/EBS dual element in the Fli-1 exon 1 [J].
Barbeau, B ;
Barat, C ;
Bergeron, D ;
Rassart, E .
ONCOGENE, 1999, 18 (40) :5535-5545
[6]   Characterization of the human and mouse Fli-1 promoter regions [J].
Barbeau, B ;
Bergeron, D ;
Beaulieu, M ;
Nadjem, Z ;
Rassart, E .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, 1996, 1307 (02) :220-232
[7]   Regulation of the megakaryocytic glycoprotein IX promoter by the oncogenic Ets transcription factor Fli-1 [J].
Bastian, LS ;
Kwiatkowski, BA ;
Breininger, J ;
Danner, S ;
Roth, G .
BLOOD, 1999, 93 (08) :2637-2644
[8]   ERYTHROLEUKEMIA INDUCTION BY FRIEND MURINE LEUKEMIA-VIRUS - INSERTIONAL ACTIVATION OF A NEW MEMBER OF THE ETS GENE FAMILY, FLI-1, CLOSELY LINKED TO C-ETS-1 [J].
BENDAVID, Y ;
GIDDENS, EB ;
LETWIN, K ;
BERNSTEIN, A .
GENES & DEVELOPMENT, 1991, 5 (06) :908-918
[9]   FRIEND VIRUS-INDUCED ERYTHROLEUKEMIA AND THE MULTISTAGE NATURE OF CANCER [J].
BENDAVID, Y ;
BERNSTEIN, A .
CELL, 1991, 66 (05) :831-834
[10]   IDENTIFICATION AND MAPPING OF A COMMON PROVIRAL INTEGRATION SITE FLI-1 IN ERYTHROLEUKEMIA-CELLS INDUCED BY FRIEND MURINE LEUKEMIA-VIRUS [J].
BENDAVID, Y ;
GIDDENS, EB ;
BERNSTEIN, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (04) :1332-1336