Expression of the AML-1 oncogene shortens the G1 phase of the cell cycle

被引:88
作者
Strom, DK
Nipp, J
Westendorf, JJ
Linggi, B
Lutterbach, B
Downing, JR
Lenny, N
Hiebert, SW
机构
[1] Vanderbilt Univ, Dept Biochem, Ingram Canc Ctr, Sch Med, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Dept Med, Ingram Canc Ctr, Sch Med, Nashville, TN 37232 USA
[3] St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA
[4] St Jude Childrens Res Hosp, Dept Tumor Cell Biol, Memphis, TN 38105 USA
关键词
D O I
10.1074/jbc.275.5.3438
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
AML-l-encoded transcription factor, AML-1B, regulates numerous hematopoietic-specific genes. Inappropriate expression of AML-1-family proteins is oncogenic in cell culture systems and in mice. To understand the oncogenic functions of AML-1, we established cell lines expressing AML-1B to examine the role of AML-1 in the cell cycle. DNA content analysis and bromodeoxyuridine pulse-chase studies indicated that entry into the S phase of the cell cycle was accelerated by up to 4 h in AML-1B-expressing 32D.3 myeloid progenitor cells as compared with control cells or cells expressing E2F-1. However, AML-1B was not able to induce continued cell cycle progression in the absence of growth factors. The DNA binding and transactivation domains of AML-1B were required for altering the cell cycle. Thus, AML-1B is the first transcription factor that affects the timing of the mammalian cell cycle.
引用
收藏
页码:3438 / 3445
页数:8
相关论文
共 46 条
[1]   Groucho-dependent and -independent repression activities of runt domain proteins [J].
Aronson, BD ;
Fisher, AL ;
Blechman, K ;
Caudy, M ;
Gergen, JP .
MOLECULAR AND CELLULAR BIOLOGY, 1997, 17 (09) :5581-5587
[2]  
ASKEW DS, 1991, ONCOGENE, V6, P1915
[3]   PEBP2-ALPHA-B/MOUSE AML1 CONSISTS OF MULTIPLE ISOFORMS THAT POSSESS DIFFERENTIAL TRANSACTIVATION POTENTIALS [J].
BAE, SC ;
OGAWA, E ;
MARUYAMA, M ;
OKA, H ;
SATAKE, M ;
SHIGESADA, K ;
JENKINS, NA ;
GILBERT, DJ ;
COPELAND, NG ;
ITO, Y .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (05) :3242-3252
[4]   CBF beta-SMMHC, expressed in M4Eo AML, reduced CBF DNA-binding and inhibited the G1 to S cell cycle transition at the restriction point in myeloid and lymphoid cells [J].
Cao, WS ;
BritosBray, M ;
Claxton, DF ;
Kelley, CA ;
Speck, NA ;
Liu, PP ;
Friedman, AD .
ONCOGENE, 1997, 15 (11) :1315-1327
[5]   The p21Cip1 and p27Kip1 CDK 'inhibitors' are essential activators of cyclin D-dependent kinases in murine fibroblasts [J].
Cheng, MG ;
Olivier, P ;
Diehl, JA ;
Fero, M ;
Roussel, MF ;
Roberts, JM ;
Sherr, CJ .
EMBO JOURNAL, 1999, 18 (06) :1571-1583
[6]   FUSION OF THE TEL GENE ON 12P13 TO THE AML1 GENE ON 21Q22 IN ACUTE LYMPHOBLASTIC-LEUKEMIA [J].
GOLUB, TR ;
BARKER, GF ;
BOHLANDER, SK ;
HIEBERT, SW ;
WARD, DC ;
BRAYWARD, P ;
MORGAN, E ;
RAIMONDI, SC ;
ROWLEY, JD ;
GILLILAND, DG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (11) :4917-4921
[7]   REGIONS OF THE RETINOBLASTOMA GENE-PRODUCT REQUIRED FOR ITS INTERACTION WITH THE E2F TRANSCRIPTION FACTOR ARE NECESSARY OF E2 PROMOTER REPRESSION AND PRB-MEDIATED GROWTH SUPPRESSION [J].
HIEBERT, SW .
MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (06) :3384-3391
[8]   THE INTERACTION OF RB WITH E2F COINCIDES WITH AN INHIBITION OF THE TRANSCRIPTIONAL ACTIVITY OF E2F [J].
HIEBERT, SW ;
CHELLAPPAN, SP ;
HOROWITZ, JM ;
NEVINS, JR .
GENES & DEVELOPMENT, 1992, 6 (02) :177-185
[9]  
HIEBERT SW, 1995, MOL CELL BIOL, V15, P6864
[10]   TLE, the human homolog of Groucho, interacts with AML1 and acts as a repressor of AML1-induced transactivation [J].
Imai, Y ;
Kurokawa, M ;
Tanaka, K ;
Friedman, AD ;
Ogawa, S ;
Mitani, K ;
Yazaki, Y ;
Hirai, H .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 252 (03) :582-589