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Realgar induces apoptosis in the chronic lymphocytic leukemia cell line MEC-1

The aim of the present study was to investigate the effect of realgar on the viability, proliferation and apoptosis in the human chronic lymphocytic leukemia (CLL) cell line, MEC-1. Potential mechanisms mediating the effect were also explored in the experiment. Cultured MEC-1 cells were incubated wi... Full description

Journal Title: Molecular Medicine Reports 12/2013, Vol.8(6), pp.1866-1870
Main Author: Liu, Xinyu
Other Authors: Li, Xianglu , Wang, Ling , Lv, Xiao , Chen, Na , Li, Peipei , Lu, Kang , Wang, Xin
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1791-2997 ; E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2013.1731
Link: http://www.spandidos-publications.com/molecular medicine reports/8/6/1866
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recordid: spandido10.3892/mmr.2013.1731
title: Realgar induces apoptosis in the chronic lymphocytic leukemia cell line MEC-1
format: Article
creator:
  • Liu, Xinyu
  • Li, Xianglu
  • Wang, Ling
  • Lv, Xiao
  • Chen, Na
  • Li, Peipei
  • Lu, Kang
  • Wang, Xin
subjects:
  • Chronic Lymphocytic Leukemia
  • Realgar
  • Apoptosis
ispartof: Molecular Medicine Reports, 12/2013, Vol.8(6), pp.1866-1870
description: The aim of the present study was to investigate the effect of realgar on the viability, proliferation and apoptosis in the human chronic lymphocytic leukemia (CLL) cell line, MEC-1. Potential mechanisms mediating the effect were also explored in the experiment. Cultured MEC-1 cells were incubated with various concentrations of realgar for 24, 48 and 72 h. A WST-8 assay was employed to evaluate the effect on cell viability. Inhibitory effects on cell proliferation were determined using a 5-bromodeoxyuridine cell proliferation ELISA. The apoptotic effect on MEC-1 cells was evaluated by annexin V-fluorescein isothiocyanate/propidium iodide dual staining, followed by flow cytometry. Quantitative polymerase chain reaction was performed to determine the mRNA expression levels of BCL2-associated X protein ( BAX ), BCL2-like 1 ( Bcl-xL) , v-myc myelocytomatosis viral oncogene homolog (avian; c-Myc ) and cyclin-dependent kinase inhibitor 1A ( p21 ). It was found that viability and proliferation were significantly reduced while apoptotic rates increased in MEC-1 cells following exposure to realgar. Furthermore, mRNA expression of BAX and c-Myc was upregulated and downregulated, respectively, in realgar-treated MEC-1 cells. In conclusion, the results showed that realgar inhibits viability and proliferation and induces apoptosis of MEC-1 cells in a dose- and time-dependent manner. The effect may depend on the mitochondrial apoptosis pathway. The results of the present study may be beneficial in the identification of a new target therapy for CLL.
language: eng
source:
identifier: ISSN: 1791-2997 ; E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2013.1731
fulltext: fulltext
issn:
  • 1791-2997
  • 17912997
  • 1791-3004
  • 17913004
url: Link


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titleRealgar induces apoptosis in the chronic lymphocytic leukemia cell line MEC-1
creatorLiu, Xinyu ; Li, Xianglu ; Wang, Ling ; Lv, Xiao ; Chen, Na ; Li, Peipei ; Lu, Kang ; Wang, Xin
ispartofMolecular Medicine Reports, 12/2013, Vol.8(6), pp.1866-1870
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subjectChronic Lymphocytic Leukemia ; Realgar ; Apoptosis
descriptionThe aim of the present study was to investigate the effect of realgar on the viability, proliferation and apoptosis in the human chronic lymphocytic leukemia (CLL) cell line, MEC-1. Potential mechanisms mediating the effect were also explored in the experiment. Cultured MEC-1 cells were incubated with various concentrations of realgar for 24, 48 and 72 h. A WST-8 assay was employed to evaluate the effect on cell viability. Inhibitory effects on cell proliferation were determined using a 5-bromodeoxyuridine cell proliferation ELISA. The apoptotic effect on MEC-1 cells was evaluated by annexin V-fluorescein isothiocyanate/propidium iodide dual staining, followed by flow cytometry. Quantitative polymerase chain reaction was performed to determine the mRNA expression levels of BCL2-associated X protein ( BAX ), BCL2-like 1 ( Bcl-xL) , v-myc myelocytomatosis viral oncogene homolog (avian; c-Myc ) and cyclin-dependent kinase inhibitor 1A ( p21 ). It was found that viability and proliferation were significantly reduced while apoptotic rates increased in MEC-1 cells following exposure to realgar. Furthermore, mRNA expression of BAX and c-Myc was upregulated and downregulated, respectively, in realgar-treated MEC-1 cells. In conclusion, the results showed that realgar inhibits viability and proliferation and induces apoptosis of MEC-1 cells in a dose- and time-dependent manner. The effect may depend on the mitochondrial apoptosis pathway. The results of the present study may be beneficial in the identification of a new target therapy for CLL.
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titleRealgar induces apoptosis in the chronic lymphocytic leukemia cell line MEC-1
descriptionThe aim of the present study was to investigate the effect of realgar on the viability, proliferation and apoptosis in the human chronic lymphocytic leukemia (CLL) cell line, MEC-1. Potential mechanisms mediating the effect were also explored in the experiment. Cultured MEC-1 cells were incubated with various concentrations of realgar for 24, 48 and 72 h. A WST-8 assay was employed to evaluate the effect on cell viability. Inhibitory effects on cell proliferation were determined using a 5-bromodeoxyuridine cell proliferation ELISA. The apoptotic effect on MEC-1 cells was evaluated by annexin V-fluorescein isothiocyanate/propidium iodide dual staining, followed by flow cytometry. Quantitative polymerase chain reaction was performed to determine the mRNA expression levels of BCL2-associated X protein ( BAX ), BCL2-like 1 ( Bcl-xL) , v-myc myelocytomatosis viral oncogene homolog (avian; c-Myc ) and cyclin-dependent kinase inhibitor 1A ( p21 ). It was found that viability and proliferation were significantly reduced while apoptotic rates increased in MEC-1 cells following exposure to realgar. Furthermore, mRNA expression of BAX and c-Myc was upregulated and downregulated, respectively, in realgar-treated MEC-1 cells. In conclusion, the results showed that realgar inhibits viability and proliferation and induces apoptosis of MEC-1 cells in a dose- and time-dependent manner. The effect may depend on the mitochondrial apoptosis pathway. The results of the present study may be beneficial in the identification of a new target therapy for CLL.
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abstractThe aim of the present study was to investigate the effect of realgar on the viability, proliferation and apoptosis in the human chronic lymphocytic leukemia (CLL) cell line, MEC-1. Potential mechanisms mediating the effect were also explored in the experiment. Cultured MEC-1 cells were incubated with various concentrations of realgar for 24, 48 and 72 h. A WST-8 assay was employed to evaluate the effect on cell viability. Inhibitory effects on cell proliferation were determined using a 5-bromodeoxyuridine cell proliferation ELISA. The apoptotic effect on MEC-1 cells was evaluated by annexin V-fluorescein isothiocyanate/propidium iodide dual staining, followed by flow cytometry. Quantitative polymerase chain reaction was performed to determine the mRNA expression levels of BCL2-associated X protein ( BAX ), BCL2-like 1 ( Bcl-xL) , v-myc myelocytomatosis viral oncogene homolog (avian; c-Myc ) and cyclin-dependent kinase inhibitor 1A ( p21 ). It was found that viability and proliferation were significantly reduced while apoptotic rates increased in MEC-1 cells following exposure to realgar. Furthermore, mRNA expression of BAX and c-Myc was upregulated and downregulated, respectively, in realgar-treated MEC-1 cells. In conclusion, the results showed that realgar inhibits viability and proliferation and induces apoptosis of MEC-1 cells in a dose- and time-dependent manner. The effect may depend on the mitochondrial apoptosis pathway. The results of the present study may be beneficial in the identification of a new target therapy for CLL.
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doi10.3892/mmr.2013.1731
date2013-12