STAT5 activation by BCR-Abl contributes to transformation of K562 leukemia cells

被引:145
作者
de Groot, RP
Raaijmakers, JAM
Lammers, JWJ
Jove, R
Koenderman, L
机构
[1] Univ Utrecht Hosp, Dept Pulm Dis, NL-3584 CX Utrecht, Netherlands
[2] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Mol Oncol Program, Tampa, FL 33612 USA
关键词
D O I
10.1182/blood.V94.3.1108.415k07_1108_1112
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Signal transducers and activators of transcription (STATs) belong to a family of transcription factors that were originally identified as mediators of cytokine-induced gene expression. Recent evidence, however, has shown that certain members of the STAT family, including STAT3, are also involved in cellular transformation. Here we show that STAT5 also plays a role in cellular transformation by the BCR-Abl oncogene. In BCR-Abl transformed K562 cells, STAT5A and 5B are constitutively phosphorylated on tyro sine and are transcriptionally active. Moreover, expression of a dominant negative form of STAT5 shows that active STAT5 is necessary for the growth in soft agar of these cells. These results show that besides STAT3, STAT5 can also be involved in cellular transformation. (C) 1999 by The American Society of Hematology.
引用
收藏
页码:1108 / 1112
页数:5
相关论文
共 43 条
[1]   BCR-ABL and constitutively active erythropoietin receptor (cEpoR) activate distinct mechanisms for growth factor-independence and inhibition of apoptosis in Ba/F3 cell line [J].
Ahmed, M ;
Dusanter-Fourt, I ;
Bernard, M ;
Mayeux, P ;
Hawley, RG ;
Bennardo, T ;
Novault, S ;
Bonnet, ML ;
Gisselbrecht, S ;
Varet, B ;
Turhan, AG .
ONCOGENE, 1998, 16 (04) :489-496
[2]   Cytokine receptor-independent, constitutively active variants of STAT5 [J].
Berchtold, S ;
Moriggl, R ;
Gouilleux, F ;
Silvennoinen, O ;
Beisenherz, C ;
Pfitzner, E ;
Wissler, M ;
Stocklin, E ;
Groner, B .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (48) :30237-30243
[3]   Stat3 activation is required for cellular transformation by v-src [J].
Bromberg, JF ;
Horvath, CM ;
Besser, D ;
Lathem, WW ;
Darnell, JE .
MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (05) :2553-2558
[4]   ACTIVATION OF THE STAT3 ACUTE-PHASE RESPONSE FACTOR TRANSCRIPTION FACTOR BY INTERLEUKIN-5 [J].
CALDENHOVEN, E ;
VANDIJK, T ;
RAAIJMAKERS, JAM ;
LAMMERS, JWJ ;
KOENDERMAN, L ;
DEGROOT, RP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (43) :25778-25784
[5]   STAT3 beta, a splice variant of transcription factor STAT3, is a dominant negative regulator of transcription [J].
Caldenhoven, E ;
vanDijk, TB ;
Solari, R ;
Armstrong, J ;
Raaijmakers, JAM ;
Lammers, JWJ ;
Koenderman, L ;
deGroot, RP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (22) :13221-13227
[6]  
Cao XM, 1996, MOL CELL BIOL, V16, P1595
[7]   Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl [J].
Carlesso, N ;
Frank, DA ;
Griffin, JD .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (03) :811-820
[8]  
Chai SK, 1997, J IMMUNOL, V159, P4720
[9]   Abrogation of interleukin-3 dependence of myeloid cells by the v-src oncogene requires SH2 and SH3 domains which specify activation of STATs [J].
Chaturvedi, P ;
Sharma, S ;
Reddy, EP .
MOLECULAR AND CELLULAR BIOLOGY, 1997, 17 (06) :3295-3304
[10]   TRANSFORMATION OF AN INTERLEUKIN-3-DEPENDENT HEMATOPOIETIC-CELL LINE BY THE CHRONIC MYELOGENOUS LEUKEMIA-SPECIFIC P210BER/ABL PROTEIN [J].
DALEY, GQ ;
BALTIMORE, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (23) :9312-9316