A zinc-finger transcription factor induced by TGF-β promotes apoptotic cell death in epithelial Mv1Lu cells

被引:90
作者
Chalaux, E
López-Rovira, T
Rosa, JL
Pons, G
Boxer, LM
Bartrons, R
Ventura, F
机构
[1] Univ Barcelona, Dept Ciencies Fisiol 2, Lhospitalet De Llobregat 08907, Spain
[2] Stanford Univ, Dept Med, Stanford, CA 94305 USA
关键词
transforming growth factor-beta; apoptosis; transcriptional regulation;
D O I
10.1016/S0014-5793(99)01051-0
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
Transforming growth factor-beta (TGF-beta) superfamily members constitute a group of multifunctional factors that are able to stimulate apoptotic cell death in a variety of cells. In this report, we show that a zinc-finger transcription factor (TIEG) is an immediate early gene transcriptionally induced by TGF-beta in the epithelial Mv1Lu cell line. We also demonstrate that, mimicking TGF-beta effects, ectopic overexpression of TIEG is sufficient to trigger the apoptotic cell program in these cells, which is preceded by a decrease of Bcl-2 protein levels, Finally, apoptotic events elicited by TIEG overexpression can be effectively prevented by ectopic co-expression of Bcl-2, On the basis of these results we suggest that induction of TIEG expression has a role in the pro-apoptotic properties of TGF-beta. (C) 1999 Federation of European Biochemical Societies.
引用
收藏
页码:478 / 482
页数:5
相关论文
共 34 条
[1]  
ABDELRAZZAK Z, 1994, MOL PHARMACOL, V46, P1100
[2]   Induction of apoptosis by DPC4, a transcriptional factor regulated by transforming growth factor-beta through stress-activated protein kinase c-Jun N-terminal kinase (SAPK/JNK) signaling pathway [J].
Atfi, A ;
Buisine, M ;
Mazars, A ;
Gespach, C .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (40) :24731-24734
[3]  
Ausubel F.M., 1992, CURRENT PROTOCOLS MO
[4]   CHARACTERIZATION OF AN EARLY GROWTH-RESPONSE GENE, WHICH ENCODES A ZINC-FINGER TRANSCRIPTION FACTOR, POTENTIALLY INVOLVED IN CELL-CYCLE REGULATION [J].
BLOK, LJ ;
GROSSMANN, ME ;
PERRY, JE ;
TINDALL, DJ .
MOLECULAR ENDOCRINOLOGY, 1995, 9 (11) :1610-1620
[5]   TYPE-I RECEPTORS SPECIFY GROWTH-INHIBITORY AND TRANSCRIPTIONAL RESPONSES TO TRANSFORMING GROWTH-FACTOR-BETA AND ACTIVIN [J].
CARCAMO, J ;
WEIS, FMB ;
VENTURA, F ;
WIESER, R ;
WRANA, JL ;
ATTISANO, L ;
MASSAGUE, J .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (06) :3810-3821
[6]   JunB is involved in the inhibition of myogenic differentiation by bone morphogenetic protein-2 [J].
Chalaux, E ;
López-Rovira, T ;
Rosa, JL ;
Bartrons, R ;
Ventura, F .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (01) :537-543
[7]   BCL-2 FAMILY: Regulators of cell death [J].
Chao, DT ;
Korsmeyer, SJ .
ANNUAL REVIEW OF IMMUNOLOGY, 1998, 16 :395-419
[8]   Conversion of Bcl-2 to a Bax-like death effector by caspases [J].
Cheng, EHY ;
Kirsch, DG ;
Clem, RJ ;
Ravi, R ;
Kastan, MB ;
Bedi, A ;
Ueno, K ;
Hardwick, JM .
SCIENCE, 1997, 278 (5345) :1966-1968
[9]   Smads:: Transcriptional activators of TGF-β responses [J].
Derynck, R ;
Zhang, Y ;
Feng, XH .
CELL, 1998, 95 (06) :737-740
[10]   Alphaviruses induce apoptosis in Bcl-2-overexpressing cells: evidence for a caspase-mediated, proteolytic inactivation of Bcl-2 [J].
Grandgirard, D ;
Studer, E ;
Monney, L ;
Belser, T ;
Fellay, I ;
Borner, C ;
Michel, MR .
EMBO JOURNAL, 1998, 17 (05) :1268-1278