Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study

Objective: We aimed to understand the molecular pathways affected by bortezomib and arsenic trioxide treatment on myelomonocytoid cell line P39. Materials and Methods: Oligonucleotide microarray platforms were used for gene expression and pathway analysis. Confirmation studies were performed using...

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Main Authors: Hakan Savlı, Sara Galimberti, Deniz Sünnetçi, Martina Canestraro, Giuseppe Palumbo, Balint Nagy, Francesco Di Raimondo, Mario Petrini
Format: Article
Language:English
Published: Galenos Publishing House 2015-09-01
Series:Turkish Journal of Hematology
Subjects:
Online Access:http://www.tjh.com.tr/jvi.aspx?pdir=tjh&plng=eng&un=TJH-78309&look4=
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author Hakan Savlı
Sara Galimberti
Deniz Sünnetçi
Martina Canestraro
Giuseppe Palumbo
Balint Nagy
Francesco Di Raimondo
Mario Petrini
author_facet Hakan Savlı
Sara Galimberti
Deniz Sünnetçi
Martina Canestraro
Giuseppe Palumbo
Balint Nagy
Francesco Di Raimondo
Mario Petrini
author_sort Hakan Savlı
collection DOAJ
description Objective: We aimed to understand the molecular pathways affected by bortezomib and arsenic trioxide treatment on myelomonocytoid cell line P39. Materials and Methods: Oligonucleotide microarray platforms were used for gene expression and pathway analysis. Confirmation studies were performed using quantitative real time PCR. Results: Bortezomib treatment has shown upregulated DIABLO and NF-κBIB (a NF-κB inhibitor) and downregulated NF-κB1, NF-κB2, and BIRC1 gene expressions. Combination treatment of the two compounds showed gene expression deregulations in concordance by the results of single bortezomib treatment. Especially, P53 was a pathway more significantly modified and a gene network centralized around the beta estradiol gene. Beta estradiol, BRCA2, and FOXA1 genes were remarkable deregulations in our findings. Conclusion: Results support the suggestions about possible use of proteasome inhibitors in the treatment of high-risk myelodysplastic syndrome (MDS). NF-κB was observed as an important modulator in leukemic transformation of MDS.
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spelling doaj.art-886f63060f644c19bb2719161c4653d82023-09-02T11:32:07ZengGalenos Publishing HouseTurkish Journal of Hematology1300-77771308-52632015-09-0132320621210.4274/tjh.2014.0058Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression StudyHakan Savlı0Sara Galimberti1Deniz Sünnetçi2Martina Canestraro3Giuseppe Palumbo4Balint Nagy5Francesco Di Raimondo6Mario Petrini7Kocaeli University Faculty of Medicine, Department of Medical Genetics, Kocaeli, TurkeyPisa University Faculty of Medicine, Department of Clinical and Experimental Medicine, Division of Hematology, Pisa, ItalyKocaeli University Faculty of Medicine, Department of Medical Genetics, Kocaeli, TurkeyPisa University Faculty of Medicine, Department of Clinical and Experimental Medicine, Division of Hematology, Pisa, ItalyCatania University Faculty of Medicine, Department of Clinical and Molecular Bio-Medicine, Division of Hematology, Catania, ItalySemmelweis University Faculty of Medicine, Department of Obstetrics and Gynecology, Budapest, HungaryCatania University Faculty of Medicine, Department of Clinical and Molecular Bio-Medicine, Division of Hematology, Catania, ItalyPisa University Faculty of Medicine, Department of Clinical and Experimental Medicine, Division of Hematology, Pisa, ItalyObjective: We aimed to understand the molecular pathways affected by bortezomib and arsenic trioxide treatment on myelomonocytoid cell line P39. Materials and Methods: Oligonucleotide microarray platforms were used for gene expression and pathway analysis. Confirmation studies were performed using quantitative real time PCR. Results: Bortezomib treatment has shown upregulated DIABLO and NF-κBIB (a NF-κB inhibitor) and downregulated NF-κB1, NF-κB2, and BIRC1 gene expressions. Combination treatment of the two compounds showed gene expression deregulations in concordance by the results of single bortezomib treatment. Especially, P53 was a pathway more significantly modified and a gene network centralized around the beta estradiol gene. Beta estradiol, BRCA2, and FOXA1 genes were remarkable deregulations in our findings. Conclusion: Results support the suggestions about possible use of proteasome inhibitors in the treatment of high-risk myelodysplastic syndrome (MDS). NF-κB was observed as an important modulator in leukemic transformation of MDS.http://www.tjh.com.tr/jvi.aspx?pdir=tjh&plng=eng&un=TJH-78309&look4=BortezomibArsenic trioxideNF-κBMDSGene expression
spellingShingle Hakan Savlı
Sara Galimberti
Deniz Sünnetçi
Martina Canestraro
Giuseppe Palumbo
Balint Nagy
Francesco Di Raimondo
Mario Petrini
Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study
Turkish Journal of Hematology
Bortezomib
Arsenic trioxide
NF-κB
MDS
Gene expression
title Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study
title_full Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study
title_fullStr Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study
title_full_unstemmed Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study
title_short Bortezomib and Arsenic Trioxide Activity on a Myelodysplastic Cell Line (P39): A Gene Expression Study
title_sort bortezomib and arsenic trioxide activity on a myelodysplastic cell line p39 a gene expression study
topic Bortezomib
Arsenic trioxide
NF-κB
MDS
Gene expression
url http://www.tjh.com.tr/jvi.aspx?pdir=tjh&plng=eng&un=TJH-78309&look4=
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