Transcriptional regulation in acute promyelocytic leukemia

被引:134
作者
Lin, RJ [1 ]
Sternsdorf, T [1 ]
Tini, M [1 ]
Evans, RM [1 ]
机构
[1] Salk Inst Biol Studies, Howard Hughes Med Inst, Gene Express Lab, La Jolla, CA 92037 USA
关键词
APL; X-RAR alpha; PML; PLZF; coreprescor; HDAC; CBP/p300; POD;
D O I
10.1038/sj.onc.1204853
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
It has been 10 years since the seminal discovery that a mutant form of a retinoid acid receptor (RAR alpha) is associated with acute promyelocytic leukemia (APL). This finding, coupled with the remarkable success of retinoic acid (RA), the natural ligand of RAR alpha, in the treatment of APL, has made APL a unique model system in the study of oncogenic conversion of transcription factors in hematological malignancies. Indeed, subsequent basic and clinical studies showed that chromosomal translocation involving the RAR alpha gene is the cytogenetic hallmark of APL and that these mutant forms of RARs are the oncogenes in APL that interfere with the proliferation and differentiation pathways controlled by both RAR and their fusion partners. However, it was not until recently that the role of aberrant transcriptional regulation in the pathogenesis of APL was revealed. In this review, we summarize the biochemical and biological mechanisms of transcriptional regulation by mutant RARs and their corresponding wild-type fusion partner PML and PLZF. These studies have been instrumental in our understanding of the process of leukemogenesis in general and have laid the scientific foundation for the novel concept of transcription therapy in the treatment of human cancer.
引用
收藏
页码:7204 / 7215
页数:12
相关论文
共 132 条
[11]   Inhibition of Daxx-mediated apoptosis by heat shock protein 27 [J].
Charette, SJ ;
Lavoie, JN ;
Lambert, H ;
Landry, J .
MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (20) :7602-7612
[12]   Nuclear receptor coactivator ACTR is a novel histone acetyltransferase and forms a multimeric activation complex with P/CAF and CBP/p300 [J].
Chen, HW ;
Lin, RJ ;
Schiltz, RL ;
Chakravarti, D ;
Nash, A ;
Nagy, L ;
Privalsky, ML ;
Nakatani, Y ;
Evans, RM .
CELL, 1997, 90 (03) :569-580
[13]   A TRANSCRIPTIONAL CO-REPRESSOR THAT INTERACTS WITH NUCLEAR HORMONE RECEPTORS [J].
CHEN, JD ;
EVANS, RM .
NATURE, 1995, 377 (6548) :454-457
[14]   Distinct leukemia phenotypes in transgenic mice and different corepressor interactions generated by promyelocytic leukemia variant fusion genes PLZF-RARα and NPM-RARα [J].
Cheng, GX ;
Zhu, XH ;
Men, XQ ;
Wang, L ;
Huang, QH ;
Jin, XL ;
Xiong, SM ;
Zhu, J ;
Guo, WM ;
Chen, JQ ;
Xu, SF ;
So, E ;
Chan, LC ;
Waxman, S ;
Zelent, A ;
Chen, GQ ;
Dong, S ;
Liu, JX ;
Chen, SJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (11) :6318-6323
[15]   The homeodomain protein NK-3 recruits Groucho and a histone deacetylase complex to repress transcription [J].
Choi, CY ;
Kim, YH ;
Kwon, HJ ;
Kim, Y .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (47) :33194-33197
[16]   IDENTIFICATION OF A DOMAIN REQUIRED FOR ONCOGENIC ACTIVITY AND TRANSCRIPTIONAL SUPPRESSION BY V-ERBA AND THYROID-HORMONE RECEPTOR-ALPHA [J].
DAMM, K ;
EVANS, RM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (22) :10668-10672
[17]   Histone deacetylase associated with mSin3A mediates repression by the acute promyelocytic leukemia-associated PLZF protein [J].
David, G ;
Alland, L ;
Hong, SH ;
Wong, CW ;
DePinho, RA ;
Dejean, A .
ONCOGENE, 1998, 16 (19) :2549-2556
[18]   THE PML-RAR-ALPHA FUSION MESSENGER-RNA GENERATED BY THE T(15-17) TRANSLOCATION IN ACUTE PROMYELOCYTIC LEUKEMIA ENCODES A FUNCTIONALLY ALTERED RAR [J].
DETHE, H ;
LAVAU, C ;
MARCHIO, A ;
CHOMIENNE, C ;
DEGOS, L ;
DEJEAN, A .
CELL, 1991, 66 (04) :675-684
[19]   The LAZ3(BCL-6) oncoprotein recruits a SMRT/mSIN3A histone deacetylase containing complex to mediate transcriptional repression [J].
Dhordain, P ;
Lin, RJ ;
Quief, S ;
Lantoine, D ;
Kerckaert, JP ;
Evans, RM ;
Albagli, O .
NUCLEIC ACIDS RESEARCH, 1998, 26 (20) :4645-4651
[20]   THE PML RETINOIC ACID RECEPTOR-ALPHA TRANSLOCATION CONVERTS THE RECEPTOR FROM AN INHIBITOR TO A RETINOIC ACID-DEPENDENT ACTIVATOR OF TRANSCRIPTION FACTOR-AP-1 [J].
DOUCAS, V ;
BROCKES, JP ;
YANIV, M ;
DETHE, H ;
DEJEAN, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (20) :9345-9349