Leukemia translocation protein PLZF inhibits cell growth and expression of cyclin A

The PLZF gene was identified by its fusion with the RARalpha locus in a therapy resistant form of acute promyelocytic leukemia (APL) associated with the t(11;17)(q23;q21) translocation. Here we describe PLZF as a negative regulator of cell cycle progression ultimately leading to growth suppression....

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Published inOncogene Vol. 18; no. 4; pp. 925 - 934
Main Authors YEYATI, P. L, SHAKNOVICH, R, BOTERASHVILI, S, JIA LI, BALL, H. J, WAXMAN, S, NASON-BURCHENAL, K, DMITROVSKY, E, ZELENT, A, LICHT, J. D
Format Journal Article
LanguageEnglish
Published Basingstoke Nature Publishing 28.01.1999
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Abstract The PLZF gene was identified by its fusion with the RARalpha locus in a therapy resistant form of acute promyelocytic leukemia (APL) associated with the t(11;17)(q23;q21) translocation. Here we describe PLZF as a negative regulator of cell cycle progression ultimately leading to growth suppression. PLZF can bind and repress the cyclin A2 promoter while expression of cyclin A2 reverts the growth suppressed phenotype of myeloid cells expressing PLZF. In contrast RARalpha-PLZF, a fusion protein generated in t(11;17)(q23;q21)-APL activates cyclin A2 transcription and allows expression of cyclin A in anchorage-deprived NIH3T3 cells. Therefore, cyclin A2 is a candidate target gene for PLZF and inhibition of cyclin A expression may contribute to the growth suppressive properties of PLZF. Deregulation of cyclin A2 by RARalpha-PLZF may represent an oncogenic mechanism of this chimeric protein and contribute to the aggressive clinical phenotype of t(11;17)(q23;q21)-associated APL.
AbstractList The PLZF gene was identified by its fusion with the RAR alpha locus in a therapy resistant form of acute promyelocytic leukemia (APL) associated with the t(11; 17)(q23; q21) translocation. Here we describe PLZF as a negative regulator of cell cycle progression ultimately leading to growth suppression. PLZF can bind and repress the cyclin A2 promoter while expression of cyclin A2 reverts the growth suppressed phenotype of myeloid cells expressing PLZF. In contrast RAR alpha -PLZF, a fusion protein generated in t(11; 17)(q23; q21)-APL activates cyclin A2 transcription and allows expression of cyclin A in anchorage-deprived NIH3T3 cells. Therefore, cyclin A2 is a candidate target gene for PLZF and inhibition of cyclin A expression may contribute to the growth suppressive properties of PLZF. Deregulation of cyclin A2 by RAR alpha -PLZF may represent an oncogenic mechanism of this chimeric protein and contribute to the aggressive clinical phenotype of t(11; 17)(q23; q21)-associated APL.
The PLZF gene was identified by its fusion with the RARalpha locus in a therapy resistant form of acute promyelocytic leukemia (APL) associated with the t(11;17)(q23;q21) translocation. Here we describe PLZF as a negative regulator of cell cycle progression ultimately leading to growth suppression. PLZF can bind and repress the cyclin A2 promoter while expression of cyclin A2 reverts the growth suppressed phenotype of myeloid cells expressing PLZF. In contrast RARalpha-PLZF, a fusion protein generated in t(11;17)(q23;q21)-APL activates cyclin A2 transcription and allows expression of cyclin A in anchorage-deprived NIH3T3 cells. Therefore, cyclin A2 is a candidate target gene for PLZF and inhibition of cyclin A expression may contribute to the growth suppressive properties of PLZF. Deregulation of cyclin A2 by RARalpha-PLZF may represent an oncogenic mechanism of this chimeric protein and contribute to the aggressive clinical phenotype of t(11;17)(q23;q21)-associated APL.
Author YEYATI, P. L
JIA LI
NASON-BURCHENAL, K
BOTERASHVILI, S
LICHT, J. D
BALL, H. J
ZELENT, A
WAXMAN, S
DMITROVSKY, E
SHAKNOVICH, R
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Issue 4
Keywords Chromosomal aberration
Human
Promyelocytic leukemia
Cell proliferation
Acute
Malignant hemopathy
Gene expression
Carcinogenesis
Cell line
Cyclin A
Cell cycle
Abnormal chromosome
Fusion protein
Hybrid gene
Chromosome translocation
Language English
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PublicationTitle Oncogene
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Snippet The PLZF gene was identified by its fusion with the RARalpha locus in a therapy resistant form of acute promyelocytic leukemia (APL) associated with the...
The PLZF gene was identified by its fusion with the RAR alpha locus in a therapy resistant form of acute promyelocytic leukemia (APL) associated with the t(11;...
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SubjectTerms 3T3 Cells
Animals
Biological and medical sciences
Cell Cycle - genetics
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Chromosomes, Human, Pair 11
Chromosomes, Human, Pair 17
Cyclin A - metabolism
Cyclin-Dependent Kinases - metabolism
DNA-Binding Proteins - genetics
DNA-Binding Proteins - physiology
Fundamental and applied biological sciences. Psychology
Genetic Vectors
Humans
Interphase - genetics
Kruppel-Like Transcription Factors
Leukemia, Promyelocytic, Acute - genetics
Leukemia, Promyelocytic, Acute - metabolism
Leukemia, Promyelocytic, Acute - pathology
Mice
Molecular and cellular biology
Neoplasm Proteins - metabolism
Oncogene Proteins, Fusion - physiology
Promyelocytic Leukemia Zinc Finger Protein
S Phase - genetics
Transcription Factors - genetics
Transcription Factors - physiology
Translocation, Genetic
Zinc Fingers - physiology
Title Leukemia translocation protein PLZF inhibits cell growth and expression of cyclin A
URI https://www.ncbi.nlm.nih.gov/pubmed/10023668
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