Triad 1 induces apoptosis by p53 activation

被引:15
作者
Jung, Jin Hyuk [1 ]
Lee, Sun-Mi [1 ]
Bae, Seunghee [1 ]
Lee, Su-Jae [2 ]
Park, In-Chul [3 ]
Jin, Young-Woo [4 ]
Lee, Jae Ho [1 ]
An, Sungkwan [1 ,5 ]
机构
[1] Konkuk Univ, Funct Genome Res Inst, Seoul 143701, South Korea
[2] Hanyang Univ, Dept Chem, Seoul 133791, South Korea
[3] Korea Inst Radiol & Med Sci, Lab Funct Genom, Seoul 139706, South Korea
[4] KHNP, Radiat Hlth Res Inst, Div Radiat Effect Res, Seoul 132703, South Korea
[5] Konkuk Univ, Venture Business Supporting Ctr, LIFEnGENE Inc, Seoul 143701, South Korea
来源
FEBS LETTERS | 2010年 / 584卷 / 08期
关键词
Triad; 1; Gfi-1; Apoptosis; p53; RING finger; UBIQUITIN LIGASE; RETINOIC ACID; DEGRADATION; CELLS; STABILIZATION; EXPRESSION; PATHWAY; GROWTH; DEATH; MDM2;
D O I
10.1016/j.febslet.2010.03.011
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
Triad 1 (2 RING [ really interesting new gene] fingers and DRIL [double RING finger linked] 1) is an E3 ligase that induces apoptosis and clonogenic inhibition in myeloid cells through Gfi-1 stabilization. Here we demonstrate that Triad 1 induces apoptosis in several cancer cell lines including MCF7, A549, U2OS, and HCT 116 p53(+/+) cells via its RING ligase activity. Interestingly, in these cancer cells, Triad 1-induced apoptosis is not mediated by Gfi-1 stabilization but is instead p53-dependent. Moreover, Triad 1 promotes transactivation of p53. These results suggest that Triad 1 can induce apoptosis through its ligase activity via p53 activation. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码:1565 / 1570
页数:6
相关论文
共 27 条
[1]   Multiple roles of the tumor suppressor p53 [J].
Bargonetti, J ;
Manfredi, JJ .
CURRENT OPINION IN ONCOLOGY, 2002, 14 (01) :86-91
[2]   Gfi-1 represses CDKN2B encoding p15INK4B through interaction with Miz-1 [J].
Basu, Suchitra ;
Liu, Qingquan ;
Qiu, Yaling ;
Dong, Fan .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2009, 106 (05) :1433-1438
[3]   Post-translational modification of p53 in tumorigenesis [J].
Bode, AM ;
Dong, ZG .
NATURE REVIEWS CANCER, 2004, 4 (10) :793-805
[4]   Ubiquitin-mediated regulation of apoptosis [J].
Broemer, Melke ;
Meier, Pascal .
TRENDS IN CELL BIOLOGY, 2009, 19 (03) :130-140
[5]   Ubiquitination, phosphorylation and acetylation: the molecular basis for p53 regulation [J].
Brooks, CL ;
Gu, W .
CURRENT OPINION IN CELL BIOLOGY, 2003, 15 (02) :164-171
[6]   p53 ubiquitination: Mdm2 and beyond [J].
Brooks, CL ;
Gu, W .
MOLECULAR CELL, 2006, 21 (03) :307-315
[7]   P53-DEPENDENT APOPTOSIS IN THE ABSENCE OF TRANSCRIPTIONAL ACTIVATION OF P53-TARGET GENES [J].
CAELLES, C ;
HELMBERG, A ;
KARIN, M .
NATURE, 1994, 370 (6486) :220-223
[8]   Runt-Related Transcription Factor RUNX3 Is a Target of MDM2-Mediated Ubiquitination [J].
Chi, Xin-Zi ;
Kim, Jiyeon ;
Lee, Yong-Hee ;
Lee, Jung-Won ;
Lee, Kyeong-Sook ;
Wee, Heejun ;
Kim, Wun-Jae ;
Park, Woo-Yoon ;
Oh, Byung-Chul ;
Stein, Gary S. ;
Ito, Yoshiaki ;
van Wijnen, Andre J. ;
Bae, Suk-Chul .
CANCER RESEARCH, 2009, 69 (20) :8111-8119
[9]   WILD-TYPE P53 ACTIVATES TRANSCRIPTION INVITRO [J].
FARMER, G ;
BARGONETTI, J ;
ZHU, H ;
FRIEDMAN, P ;
PRYWES, R ;
PRIVES, C .
NATURE, 1992, 358 (6381) :83-86
[10]  
FINLEY D, 1991, ANNU REV CELL BIOL, V7, P25, DOI 10.1146/annurev.cb.07.110191.000325